157 results on '"Billaud, Marie"'
Search Results
2. Abstract 11993: Integrative Analysis of Single-Cell Transcriptomics and Polygenic Risk Scores Uncovers Vascular Smooth Muscle Cell Heterogeneity in Human Aortic Aneurisms
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Pepin, Mark E, Vellari, S.K., Atri, D.S., Reddy, Ankith, Sias-Garcia, Oscar, Hamel, Andrew R, Billaud, Marie, Lee-Kim, Vivian, Segre, Ayellet, and Gupta, Rajat
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- 2023
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3. Aortic Dissection is Determined by Specific Shape and Hemodynamic Interactions
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Williams, Jessica G., Marlevi, David, Bruse, Jan L., Nezami, Farhad R., Moradi, Hamed, Fortunato, Ronald N., Maiti, Spandan, Billaud, Marie, Edelman, Elazer R., and Gleason, Thomas G.
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- 2022
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4. Only the strong "aorta" survives: the female edge in a mouse model of severe Marfan syndrome.
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Billaud, Marie and Phillippi, Julie A.
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VASCULAR resistance , *SEX factors in disease , *ASCENDING aorta aneurysms , *THORACIC aneurysms , *AORTIC root aneurysms , *AORTIC dissection , *PREMATURE menopause - Abstract
Marfan syndrome is a connective tissue disorder that affects multiple organs, with the most serious complications occurring in the cardiovascular system. Aortic root dilatation and dissection are particularly concerning. While the prevalence of Marfan syndrome is equal between genders, male patients have a higher risk of developing thoracic aortic aneurysm and dissection compared to females. A recent study using a mouse model of severe Marfan syndrome found that male mice had poorer survival rates and exhibited lower elastin content and more fragmented elastic fibers compared to female mice. The study suggests that material properties, aortic size, and wall integrity may be connected to dissection risk. Further research is needed to understand how age and sex contribute to dissection risk in Marfan syndrome. [Extracted from the article]
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- 2024
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5. Multifocal electroretinogram findings in sickle cell maculopathy
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Beral, Laurence, Romana, Marc, Lemonne, Nathalie, Garnier, Yoann, Billaud, Marie, Acomat, Malik, Zorobabel, Coralie, Etienne-Julan, Maryse, David, Thierry, and Connes, Philippe
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- 2019
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6. Predissection-derived geometric and distensibility indices reveal increased peak longitudinal stress and stiffness in patients sustaining acute type A aortic dissection: Implications for predicting dissection
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Emerel, Leonid, Thunes, James, Kickliter, Trevor, Billaud, Marie, Phillippi, Julie A., Vorp, David A., Maiti, Spandan, and Gleason, Thomas G.
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- 2019
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7. Androgenic steroids induce pathologic scarring in a preclinical porcine model via dysfunctional extracellular matrix deposition.
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Reiche, Erik, Keller, Patrick R., Soares, Vance, Schuster, Calvin R., Rahmayanti, Siti, Mroueh, Jessica, Mroueh, Vanessa, Billaud, Marie, Hu, Sophia, Hoover‐Watson, Hunter, Lian, Christine G., Tan, Yu, Doloff, Joshua C., Newell‐Fugate, Annie E., and Coon, Devin
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- 2024
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8. Substance use disorder of equimolar oxygen-nitrous oxide mixture in French sickle-cell patients: results of the PHEDRE study.
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Gérardin, Marie, Rousselet, Morgane, Couec, Marie-Laure, Masseau, Agathe, Chantalat, Christelle, Driss, Françoise, Guitton, Corinne, Debbache, Karima, Foïs, Elena, Galacteros, Frédéric, Habibi, Anoosha, Léon, Anne, Mattioni, Sarah, Santin, Aline, Alexis-Fardini, Scylia, Augusty, Edima, Billaud, Marie, Divialle-Doumdo, Lydia, Etienne-Julan, Maryse, and Lemonne, Nathalie
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SUBSTANCE abuse ,ANALGESICS ,SICKLE cell anemia ,GAS mixtures ,NITROUS oxide ,PSEUDOADDICTION ,HOSPITAL patients - Abstract
Background: In many countries, nitrous oxide is used in a gas mixture (EMONO) for short-term analgesia. Cases of addiction, with significant misuse, have been reported in hospitalized patients. Patients suffering from sickle cell disease (SCD) could represent a high-risk population for substance use disorder (SUD) due to their significant pain crisis and repeated use of EMONO. The objective of the PHEDRE study was to assess the prevalence of SUD for EMONO in French SCD patients. Results: A total of 993 patients were included. Among 339 EMONO consumers, only 38 (11%) had a SUD, with very few criteria, corresponding mainly to a mild SUD due to a use higher than expected (in quantity or duration) and relational tensions with the care teams. Almost all patients (99.7%) were looking for an analgesic effect, but 68% of patients were also looking for other effects. The independent risks factors associated with at least one SUD criterion were: the feeling of effects different from the expected therapeutic effects of EMONO, at least one hospitalization for vaso occlusive crisis in the past 12 months and the presence of a SUD for at least one other analgesic drug. Conclusions: The use of EMONO was not problematic for the majority of patients. Manifestations of SUD that led to tensions with healthcare teams should alert and lead to an evaluation, to distinguish a true addiction from a pseudoaddiction which may be linked to an insufficient analgesic treatment related to an underestimation of pain in SCD patients. Trial registration: Clinical Trials, NCT02580565. Registered 16 October 2015, https://clinicaltrials.gov/ [ABSTRACT FROM AUTHOR]
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- 2024
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9. Perivascular extracellular matrix hydrogels mimic native matrix microarchitecture and promote angiogenesis via basic fibroblast growth factor
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Fercana, George R., Yerneni, Saigopalakrishna, Billaud, Marie, Hill, Jennifer C., VanRyzin, Paul, Richards, Tara D., Sicari, Brian M., Johnson, Scott A., Badylak, Stephen F., Campbell, Phil G., Gleason, Thomas G., and Phillippi, Julie A.
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- 2017
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10. 48 - Vascular Physiology
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Billaud, Marie, Sabe, Ashraf A., Harrison, David G., and Sellke, Frank W.
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- 2024
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11. Elevated oxidative stress in the aortic media of patients with bicuspid aortic valve
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Billaud, Marie, Phillippi, Julie A., Kotlarczyk, Mary P., Hill, Jennifer C., Ellis, Bradley W., St Croix, Claudette M., Cantu-Medéllin, Nadiezhda, Kelley, Eric E., and Gleason, Thomas G.
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- 2017
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12. Adventitia-derived extracellular matrix hydrogel enhances contractility of human vasa vasorum-derived pericytes via α(2)β(1) integrin and TGFβ receptor
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Wintruba, Kaitlyn L., Hill, Jennifer C., Richards, Tara D., Lee, Yoojin C., Kaczorowski, David J., Sultan, Ibrahim, Badylak, Stephen F., Billaud, Marie, Gleason, Thomas G., and Phillippi, Julie A.
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Adventitia ,Integrins ,Swine ,Transforming Growth Factor beta ,Vasa Vasorum ,Animals ,Humans ,Biocompatible Materials ,Hydrogels ,Pericytes ,Article ,Collagen Type I ,Extracellular Matrix - Abstract
Pericytes are essential components of small blood vessels and are found in human aortic vasa vasorum. Prior work uncovered lower vasa vasorum density and decreased levels of pro-angiogenic growth factors in adventitial specimens of human ascending thoracic aortic aneurysm. We hypothesized that adventitial extracellular matrix (ECM) from normal aorta promotes pericyte function by increasing pericyte contractile function through mechanisms deficient in ECM derived from aneurysmal aortic adventitia. ECM biomaterials were prepared as lyophilized particulates from decellularized adventitial specimens of human and porcine aorta. Immortalized human aortic adventitia-derived pericytes were cultured within Type I collagen gels in the presence or absence of human or porcine adventitial ECMs. Cell contractility index was quantified by measuring the gel area immediately following gelation and after 48 h of culture. Normal human and porcine adventitial ECM increased contractility of pericytes when compared with pericytes cultured in absence of adventitial ECM. In contrast, aneurysm-derived human adventitial ECM failed to promote pericyte contractility. Pharmacological inhibition of TGFβR1 and antibody blockade of α(2)β(1) integrin independently decreased porcine adventitial ECM-induced pericyte contractility. By increasing pericyte contractility, adventitial ECM may improve microvascular function and thus represents a candidate biomaterial for less invasive and preventative treatment of human ascending aortic disease.
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- 2022
13. Amount of Pannexin 1 in Smooth Muscle Cells Regulates Sympathetic Nerve-Induced Vasoconstriction.
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Dunaway, Luke S., Billaud, Marie, Macal, Edgar, Good, Miranda E., Medina, Christopher B., Lorenz, Ulrike, Ravichandran, Kodi, Koval, Michael, and Isakson, Brant E.
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Background: Panx1 (pannexin 1) forms high conductance channels that secrete ATP upon stimulation. The role of Panx1 in mediating constriction in response to direct sympathetic nerve stimulation is not known. Additionally, it is unknown how the expression level of Panx1 in smooth muscle cells (SMCs) influences α-adrenergic responses. We hypothesized that the amount of Panx1 in SMCs dictates the levels of sympathetic constriction and blood pressure.Methods: To test this hypothesis, we used genetically modified mouse models enabling expression of Panx1 in vascular cells to be varied. Electrical field stimulation on isolated arteries and blood pressure were assessed.Results: Genetic deletion of SMC Panx1 prevented constriction by electric field stimulation of sympathetic nerves. Conversely, overexpression of Panx1 in SMCs using a ROSA26 transgenic model increased sympathetic nerve-mediated constriction. Cx43 hemichannel inhibitors did not alter constriction. Next, we evaluated the effects of altered SMC Panx1 expression on blood pressure. To do this, we created mice combining a global Panx1 deletion, with ROSA26-Panx1 under the control of an inducible SMC specific Cre (Myh11). This resulted in mice that could express only human Panx1, only in SMCs. After tamoxifen, these mice had increased blood pressure that was acutely decreased by the Panx1 inhibitor spironolactone. Control mice genetically devoid of Panx1 did not respond to spironolactone.Conclusions: These data suggest Panx1 in SMCs could regulate the extent of sympathetic nerve constriction and blood pressure. The results also show the feasibility humanized Panx1-mouse models to test pharmacological candidates. [ABSTRACT FROM AUTHOR]- Published
- 2023
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14. Pannexin 1 in the Regulation of Vascular Tone
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Billaud, Marie, Sandilos, Joanna K., and Isakson, Brant E.
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- 2012
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15. A simple stabilized finite element method for solving two phase compressible–incompressible interface flows
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Billaud, Marie, Gallice, Gérard, and Nkonga, Boniface
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- 2011
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16. Spontaneous Lung Dysfunction and Fibrosis in Mice Lacking Connexin 40 and Endothelial Cell Connexin 43
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Koval, Michael, Billaud, Marie, Straub, Adam C., Johnstone, Scott R., Zarbock, Alexander, Duling, Brian R., and Isakson, Brant E.
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- 2011
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17. Vascular biomechanical properties in mice with smooth muscle specific deletion of Ndst1
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Adhikari, Neeta, Billaud, Marie, Carlson, Marjorie, Lake, Spencer P., Montaniel, Kim Ramil C., Staggs, Rod, Guan, Weihua, Walek, Dinesha, Desir, Snider, Isakson, Brant E., Barocas, Victor H., and Hall, Jennifer L.
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- 2014
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18. Adventitia‐derived extracellular matrix hydrogel enhances contractility of human vasa vasorum‐derived pericytes via α2β1 integrin and TGFβ receptor.
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Wintruba, Kaitlyn L., Hill, Jennifer C., Richards, Tara D., Lee, Yoojin C., Kaczorowski, David J., Sultan, Ibrahim, Badylak, Stephen F., Billaud, Marie, Gleason, Thomas G., and Phillippi, Julie A.
- Abstract
Pericytes are essential components of small blood vessels and are found in human aortic vasa vasorum. Prior work uncovered lower vasa vasorum density and decreased levels of pro‐angiogenic growth factors in adventitial specimens of human ascending thoracic aortic aneurysm. We hypothesized that adventitial extracellular matrix (ECM) from normal aorta promotes pericyte function by increasing pericyte contractile function through mechanisms deficient in ECM derived from aneurysmal aortic adventitia. ECM biomaterials were prepared as lyophilized particulates from decellularized adventitial specimens of human and porcine aorta. Immortalized human aortic adventitia‐derived pericytes were cultured within Type I collagen gels in the presence or absence of human or porcine adventitial ECMs. Cell contractility index was quantified by measuring the gel area immediately following gelation and after 48 h of culture. Normal human and porcine adventitial ECM increased contractility of pericytes when compared with pericytes cultured in absence of adventitial ECM. In contrast, aneurysm‐derived human adventitial ECM failed to promote pericyte contractility. Pharmacological inhibition of TGFβR1 and antibody blockade of α2β1 integrin independently decreased porcine adventitial ECM‐induced pericyte contractility. By increasing pericyte contractility, adventitial ECM may improve microvascular function and thus represents a candidate biomaterial for less invasive and preventative treatment of human ascending aortic disease. [ABSTRACT FROM AUTHOR]
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- 2022
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19. Layer-specific Nos3 expression and genotypic distribution in bicuspid aortic valve aortopathy.
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Hill, Jennifer C, Billaud, Marie, Richards, Tara D, Kotlarczyk, Mary P, Shiva, Sruti, Phillippi, Julie A, and Gleason, Thomas G
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AORTIC valve , *GENOTYPES , *SINGLE nucleotide polymorphisms , *TRICUSPID valve , *TISSUE adhesions , *AORTIC valve transplantation , *MITRAL valve - Abstract
Open in new tab Download slide OBJECTIVES We hypothesized that expression and activity of nitric oxide synthase-3 enzyme (Nos3) in bicuspid aortic valve (BAV) aortopathy are related to tissue layer and Nos3 genotype. METHODS Gene expression of Nos3 and platelet and endothelial cell adhesion molecule-1 (Pecam1) and NOS activity were measured in intima-containing media and adventitial specimens of ascending aortic tissue. The presence of 2 Nos3 single-nucleotide polymorphisms (SNPs; −786T/C and 894G/T) was determined for non-aneurysmal (NA) and aneurysmal patients with BAV (n = 40, 89, respectively); patients with tricuspid aortic valve (TAV) and aneurysm (n = 151); and NA patients with TAV (n = 100). RESULTS Elevated Nos3 relative to Pecam1 and reduced Pecam1 relative to a housekeeping gene were observed within intima-containing aortic specimens from BAV patients when compared with TAV patients. Lower Nos3 in the adventitia of aneurysmal specimens was noted when compared with specimens of NA aorta, independent of valve morphology. NOS activity was similar among cohorts in media/intima and decreased in the diseased adventitia, relative to control patients. Aneurysmal BAV patients exhibited an under-representation of the wild-type genotype for −786 SNP. No differences in genotype distribution were noted for 894 SNP. Primary intimal endothelial cells from patients with at least 1 C allele at −786 SNP exhibited lower Nos3 when compared with wild-type cells. CONCLUSIONS These findings of differential Nos3 in media/intima versus adventitia depending on valve morphology or aneurysm reveal new information regarding aneurysmal pathophysiology and support our ongoing assertion that there are distinct mechanisms giving rise to ascending aortopathy in BAV and TAV patients. [ABSTRACT FROM AUTHOR]
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- 2022
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20. Contributors
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Abbott, Brian G., Abbott, J. Dawn, Adams, David H., Alarcon, Emilio I., Al-Atassi, Talal, Al-Dameh, Ali, Allen, Mark S., Altorki, Nasser K., Anderson, Robert H., Anraku, Masaki, Antonoff, Mara B., Anyanwu, Anelechi C., M. Argote-Greene, Luis, B. Atkinson, Douglas, Awtry, Eric Herschel, Ayalon, Nir, Bacha, Emile A., Bagai, Jayant, Baillot, Richard, Baird, Christopher W., Wyler von Ballmoos, Moritz C., Barron, David J., Bavaria, Joseph E., J. Benoit, Patrick, Bernal, Jose M., P. Bichell, David, Billaud, Marie, Mahmood, Syed Usman Bin, Boodhwani, Munir, Bostock, Ian C., Bradley, Matthew J., Brawn, William J., Brizard, Christian P., Brothers, Julie A., Brown, Alana, Brown, Morgan Leigh, Bueno, Raphael, Burkhart, Harold M., Burns, Daniel J.P., Burt, Bryan M., Callahan, Ryan M., Cannon, Jeremy W., Capaccione, Kathleen M., Castelvecchio, Serenella, J. Cerfolio, Robert, Chaikof, Elliot L., Cham, Matthew D., Chang, Stephanie H., Chauvette, Vincent, Chin, Cynthia S., Chiu, Peter, Choi, Perry S, Clarke, John-Ross D, Cleveland, Joseph C., Colson, Yolonda L., Cohn, William E., Cook, Andrew C., Coselli, Joseph S., Coster, Jenalee N., Cui, Hao, Dagenais, Francois, Damiano, Ralph J., D'Amico, Thomas A., David, Tirone E., d'Avila, Andre, Azevedo, MD, Ivan Salgado de, Dearani, Joseph A., del Nido, Pedro J., Demehri, Farokh R., Demers, Philippe, Demmy, Todd Lyle, Dexter, Elisabeth U., Dezube, Aaron R., Dhupar, Rajeev, DiMaio, J. Michael, DiMaria, Matthew Christopher, DiNardo, James A., Doenst, Torsten, Dolan, Daniel Powell, Duarte, Paula, d'Udekem, Yves, Edelman, J. James, Ehsan, Afshin, Eickhoff, Emily R., Elde, Stefan, El Khoury, Gebrine, Elmadhun, Nassrene, Emani, Sitaram M., Fatima, Huma, Fauza, Dario O., Feins, Eric Norton, Feldman, Hope A., Figueroa, Paula Ugalde, Freeman, Rosario V., Friedberg, Joseph S., Fynn-Thompson, Francis, Gaudino, Mario F.L., Gaynor, J. William, Ge, Liang, Geraci, Travis C., Gergen, Anna K., Geva, Tal, Ghadimi, Kamrouz, Ghanayem, Nancy S., Ghanta, Ravi K., Gillinov, A. Marc, Glower, Donald D., Goldstone, Andrew B., Gregor, Alexander, Grimm, Joshua C., Groner, Lauren K., Grover, Frederick L., Guariento, Alvise, Guccione, Julius, Guimaron, Samantha, Gunasingha, Rathnayaka M. Kalpanee D., Halas, Monika, Hammer, Peter E., Hammon, John W., Guo, Ming Hao, Harris, Andrew W., Harrison, David G., Hauser, Thomas H., Heiden, Brendan T., Henschke, Claudia I., Hiesinger, William, Hoang, Chuong D., Hobbs, Reilly D., Hoffman, George M., Hofstetter, Wayne L., Hoganson, David M., Hraska, Viktor, Hughes, G. Chad, Hussien, Amira, Bao, Giang Thanh Huynh, Ibrahim, Marina, Iyengar, Ajay J., Jaklitsch, Michael T., Jennings, Russell, Jones, David R., Jordan, Sean A., Juraszek, Amy L., Kaiser, Larry R., Kaku, Yuji, Kaproth-Joslin, Katherine, Kays, David W., Kaza, Aditya K., Kent, Amie J., Kernstine, Kemp H., Keshavjee, Shaf, KÖksoy, Cuneyt, Kurlansky, Paul, Kwon, Michael H., Larnard, Emily A., LaPar, Damien J., Lau, Christopher, LeMaire, Scott A., Levitsky, Sidney, Levy, Jerrold H., Liang, Patric, Lighter, Melani K., Linden, Philip A., Liptay, Michael J., Litle, Virginia R., Locke, Andrew H., Luketich, James D., Lytle, Bruce W., Mack, Michael J., Madani, Michael M., Mahmood, Feroze, Maisano, Francesco, Mallidi, Hari R., Mamoun, Negmeldeen, Mangi, Abeel A., Manning, Warren J., Marshall, M. Blair, Mason, David P., Mathisen, Douglas J., Matte, Gregory S., Mattox, Kenneth L., Matyal, Robina, McCully, James D., McGilvray, Martha M.O., McKenna, Robert J., McLennan, Daniel, Menicanti, Lorenzo, Mestres, Carlos A., Meyers, Bryan F., Miller, Daniel L., Miller, D. Craig, Miller, Meagan M., Mitchell, John D., Mufarrih, Syed Hamza, Murthy, Raghav A., Naka, Yoshifumi, Nathan, Meena, Newman, Kurt, Ngu, Janet M.C., O'Connor, Michael C., Odegard, Kirsten C., Oliveira, Ricardo, H. Olsen, Griffin, Orozco-Sevilla, Vicente, Ott, Harald C., Ouzounian, Maral, Padalino, Massimo, Pahwa, Siddharth V., Paul, Subroto, Palmeri, Nicholas O., Pandi, Dimosthenis, Patterson, G. Alexander, Perry, Yaron, Petrosyan, Mikael, Pettersson, Gosta B., Piana, Robert N., Piechura, Laura M., Pinto, Duane S., Polhemus, Emily, Pomar, Jose L., Pommerening, Matthew J., Porras, Diego, Preventza, Ourania, Pua, Bradley B., Puri, Varun, Qureshi, Saqib H., Quinonez, Luis G., Raman, Vignesh, Randhawa, Simran K., Ratcliffe, Mark, Reardon, Michael J., Reilly, John J., Rekhtman, Natasha, Revels, Jonathan W., Rhodin, Kristen E., Rice, David C., Rinewalt, Daniel E., Robinson, Kortney, Rocco, Gaetano, Rocco, Raffaele, Rokosh, Rae, Romano, Jennifer C., Roy, Nathalie, Rubens, Fraser D., Ruel, Marc, Ruiz-Solano, Elyan, Rusch, Valerie W., Saad, Marwan, Sabe, Ashraf A., Salvatore, Mary M., Sanders, Stephen P., Schaff, Hartzell V., Schaheen, Lara W., Schidlow, David, Schulz, Noah E., Scrimgeour, Laura A., Scully, Brandi Braud, Seder, Christopher W., Sellke, Frank W., Sengupta, Aditya, Sepesi, Boris, Shah, Adil Aijaz, Shahani, Rohit, Shamberger, Robert C., Shih, Emily, Shrager, Joseph B., Shudo, Yasuhiro, Sideris, Antonios, Singh, Steve K., Slaughter, Mark S., Smith, Craig R., Smith, Peter K., Smithers, Charles J., Sodha, Neel R., Solaro, R. John, Sotiropoulos, Georgios, Squiers, John J., Stephens, Elizabeth H., Stewart, Shelby J., Suri, Rakesh M., Suuronen, Erik J., Svensson, Lars G., Swanson, Scott J., Sweeney, Joseph C., Szeto, Wilson Y., Taggart, David, Takaya, Hiroki, Takeda, Koji, F. Tapias, Luis, Tapias, Leonidas, Taramasso, Maurizio, Thiagarajan, Ravi R., Thistlethwaite, Patricia A., Thourani, Vinod, Tompkins, Bryon A., Tong, Michael Z., Towe, Christopher, Triphuridet, Natthaya, Truesdell, Alexander G., Tuttle, Mark K., Tweddell, James Scott, Unai, Shinya, Urschel, Harold C., Valente, Anne Marie, Vallabhajosyula, MD, Prashanth, Vander, Pluym, Christina, Vargo, Patrick R., Vekstein, Andrew M., Vieira, Arthur, Vida, Vladimiro, Vijayakumar, Shilpa, Vlahakas, Gus, Voisine, Pierre, Wadowski, Benjamin, Wall, Matthew J., Wallace, Arthur W., Walsh, Garrett L., Wang, Vicky Y., Wang, Vivian, Wee, Jon O., Welsby, Ian, Wells, Dennis A., White, Abby, Wiener, Daniel C., Wierup, Per, Williams, Judson B., Winlaw, David S., Witten, James C., Wojnarski, Charles M., Wolska, Beata M., Woo, Y. Joseph, Wu, Fred M., Yang, Stephen C., Yasufuku, Kazuhiro, Yates, Tari-Ann, Zendejas, Benjamin, Zimetbaum, Peter J., and Zhang, Dongning
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- 2024
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21. Superoxide Generation and Oxidative Tissue Damage in Bicuspid Aortic Valve-Associated Aortopathy: 104
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Phillippi, Julie A, Green, Benjamin R, Kotlarczyk, Mary P, Hermmann, Riley M, Billaud, Marie, Hill, Jennifer C, Velayutham, Murugesan, Cardounel, Arturo J, Cantu-Medéllin, Nandiezhda, Kelley, Eric E, and Gleason, Thomas G
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- 2014
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22. Expression Profile of Superoxide Dismutases and NADPH Oxidases Varies with Smooth Muscle Cell Phenotype in Thoracic Aortic Aneurysm: 73
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Billaud, Marie, Phillippi, Julie A, and Gleason, Thomas G
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- 2014
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23. Endothelial cell expression of haemoglobin α regulates nitric oxide signalling
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Straub, Adam C., Lohman, Alexander W., Billaud, Marie, Johnstone, Scott R., Dwyer, Scott T., Lee, Monica Y., Bortz, Pamela Schoppee, Best, Angela K., Columbus, Linda, Gaston, Benjamin, and Isakson, Brant E.
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- 2012
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24. Loss of Compliance in Small Arteries, but Not in Conduit Arteries, After 6 Weeks Exposure to High Fat Diet
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Billaud, Marie, Johnstone, Scott R., and Isakson, Brant E.
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- 2012
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25. Smooth Muscle Specific Deletion of Ndst1 Leads to Decreased Vessel Luminal Area and No Change in Blood Pressure in Conscious Mice
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Montaniel, Kim Ramil C., Billaud, Marie, Graham, Cassandra, Kim, Sun K., Carlson, Marjorie, Zeng, William, Zeng, Orien, Pan, Wei, Isakson, Brant E., Hall, Jennifer L., and Adhikari, Neeta
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- 2012
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26. Posttranslational Modifications in Connexins and Pannexins
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Johnstone, Scott R., Billaud, Marie, Lohman, Alexander W., Taddeo, Evan P., and Isakson, Brant E.
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- 2012
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27. The influence of gap junction network complexity on pulmonary artery smooth muscle reactivity in normoxic and chronically hypoxic conditions
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Gosak, Marko, Guibert, Christelle, Billaud, Marie, Roux, Etienne, and Marhl, Marko
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- 2014
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28. 23. Single Cell Sequencing Reveals Androgens Drive Monocyte-lineage Cell Clusters Towards Pro-inflammatory And Pro-angiogenic Transcriptomic States.
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Rahmayanti, Siti, Reiche, Erik, Hu, Sophia, Soares, Vance, Billaud, Marie, Lian, Christine G., and Coon, Devin
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- 2024
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29. 05. Temporal Progression of Sex Hormone-mediated Immune Shifts and ECM Deposition During Wound Repair.
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Rahmayanti, Siti, Reiche, Erik, Hu, Sophia, Soares, Vance, Hoover-Watson, Hunter, Mroueh, Vanessa, Mroueh, Jessica, Billaud, Marie, Lian, Christine G., and Coon, Devin
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- 2024
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30. 2. Multi-omic Analysis Defines Androgen-induced Alterations in the Balance of Innate/adaptive Immune Cell Trajectories that Induce Fibrotic Healing during Wound Repair.
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Reiche, Erik, Rahmayanti, Siti, Soares, Vance, Hu, Sophia, Hoover-Watson, Hunter, Billaud, Marie, Mroueh, Vanessa, Mroueh, Jessica, Lian, Christine G., Orgill, Dennis P., and Coon, Devin
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- 2024
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31. Expression of Pannexin Isoforms in the Systemic Murine Arterial Network
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Lohman, Alexander W., Billaud, Marie, Straub, Adam C., Johnstone, Scott R., Best, Angela K., Lee, Monica, Barr, Kevin, Penuela, Silvia, Laird, Dale W., and Isakson, Brant E.
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- 2012
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32. Mechanisms of ATP release and signalling in the blood vessel wall
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Lohman, Alexander W., Billaud, Marie, and Isakson, Brant E.
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- 2012
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33. Oxidative stress, inflammation, blood rheology, and microcirculation in adults with sickle cell disease: Effects of hydroxyurea treatment and impact of sickle cell syndrome.
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Connes, Philippe, Möckesch, Berenike, Tudor Ngo Sock, Emilienne, Hardy‐Dessources, Marie‐Dominique, Reminy, Karen, Skinner, Sarah, Billaud, Marie, Nader, Elie, Tressieres, Benoit, Etienne‐Julan, Maryse, Guillot, Nicolas, Lemonne, Nathalie, Hue, Olivier, Romana, Marc, and Antoine‐Jonville, Sophie
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SICKLE cell anemia ,HEMORHEOLOGY ,OXIDATIVE stress ,BLOOD viscosity ,MICROCIRCULATION - Abstract
Inflammation and oxidative stress play a key role in the pathophysiology of sickle cell disease (SCD). However, the potential influence of different sickle genotypes, or hydroxyurea (HU) treatment, on these factors remains poorly documented. The present study compared several plasma markers of inflammation and oxidative stress, as well as microvascular function, between patients with sickle SC disease (HbSC, n = 19) and patients with sickle cell anemia (HbSS) under hydroxyurea (HU) treatment (n = 16), or not (n = 13). Hemorheological parameters and levels of inflammatory (IL‐6, IL‐8, IFN‐γ, MCP‐1, MIP‐1β, TNF‐α) and oxidative stress (AOPP, MDA, MPO) markers were determined. Peripheral microcirculatory cutaneous blood flow and immediate microvascular response to local heat were evaluated using laser Doppler flowmetry. Oxidative stress and inflammation were lower in HbSC patients and HbSS patients under HU therapy compared to HbSS patients not treated with HU. Blood viscosity was higher in HbSC than in HbSS patients treated with or not with HU. Vasodilation response of the cutaneous microcirculation to heat stress was higher in HbSS patients receiving HU treatment. Our results clearly established that both sickle cell genotype and HU treatment modulate inflammation and oxidative stress. [ABSTRACT FROM AUTHOR]
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- 2021
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34. 22. Design And Optimization of Topical Therapeutics For Androgen/ Estrogen Receptor-based Modulation of Tissue Repair.
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Reiche, Erik, Hoover-Watson, Hunter, Soares, Vance, Rahmayanti, Siti, Mroueh, Vanessa, Mroueh, Jessica, Hu, Sophia, Billaud, Marie, Lian, Christine, Kirtane, Ameya R., and Coon, Devin
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- 2024
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35. Posttranslational Modifications in Connexins and Pannexins
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Johnstone, Scott, Billaud, Marie, Lohman, Alexander, Taddeo, Evan, and Isakson, Brant
- Abstract
Posttranslational modification is a common cellular process that is used by cells to ensure a particular protein function. This can happen in a variety of ways, e.g., from the addition of phosphates or sugar residues to a particular amino acid, ensuring proper protein life cycle and function. In this review, we assess the evidence for ubiquitination, glycosylation, phosphorylation, S-nitrosylation as well as other modifications in connexins and pannexin proteins. Based on the literature, we find that posttranslational modifications are an important component of connexin and pannexin regulation
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- 2018
36. Role of the gap junctions in the contractile response to agonists in pulmonary artery from two rat models of pulmonary hypertension
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Dahan Diana, Billaud Marie, Marthan Roger, Savineau Jean-Pierre, and Guibert Christelle
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pulmonary hypertension ,gap junctions ,connexin ,vasoreactivity ,chronic hypoxia ,monocrotaline ,connexin-mimetic peptides ,Diseases of the respiratory system ,RC705-779 - Abstract
Background Pulmonary hypertension (PH) is characterized by arterial vascular remodelling and alteration in vascular reactivity. Since gap junctions are formed with proteins named connexins (Cx) and contribute to vasoreactivity, we investigated both expression and role of Cx in the pulmonary arterial vasoreactivity in two rat models of PH. Methods Intrapulmonary arteries (IPA) were isolated from normoxic rats (N), rats exposed to chronic hypoxia (CH) or treated with monocrotaline (MCT). RT-PCR, Western Blot and immunofluorescent labelling were used to study the Cx expression. The role of Cx in arterial reactivity was assessed by using isometric contraction and specific gap junction blockers. Contractile responses were induced by agonists already known to be involved in PH, namely serotonin, endothelin-1 and phenylephrine. Results Cx 37, 40 and 43 were expressed in all rat models and Cx43 was increased in CH rats. In IPA from N rats only, the contraction to serotonin was decreased after treatment with 37-43Gap27, a specific Cx-mimetic peptide blocker of Cx 37 and 43. The contraction to endothelin-1 was unchanged after incubation with 40Gap27 (a specific blocker of Cx 40) or 37-43Gap27 in N, CH and MCT rats. In contrast, the contraction to phenylephrine was decreased by 40Gap27 or 37-43Gap27 in CH and MCT rats. Moreover, the contractile sensitivity to high potassium solutions was increased in CH rats and this hypersensitivity was reversed following 37-43Gap27 incubation. Conclusion Altogether, Cx 37, 40 and 43 are differently expressed and involved in the vasoreactivity to various stimuli in IPA from different rat models. These data may help to understand alterations of pulmonary arterial reactivity observed in PH and to improve the development of innovative therapies according to PH aetiology.
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- 2011
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37. Central Role of P2Y6 UDP Receptor in Arteriolar Myogenic ToneHighlights
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Kauffenstein, Gilles, Tamareille, Sophie, Prunier, Fabrice, Roy, Charlotte, Ayer, Audrey, Toutain, Bertrand, Billaud, Marie, Isakson, Brant, Grimaud, Linda, Loufrani, Laurent, Rousseau, Pascal, Abraham, Pierre, Procaccio, Vincent, Monyer, Hannah, de Wit, Cor, Boeynaems, Jean-Marie, Robaye, Bernard, Kwak, Brenda, Henrion, Daniel, Biologie Neurovasculaire et Mitochondriale Intégrée (BNMI), Centre National de la Recherche Scientifique (CNRS)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université d'Angers (UA), Cardioprotection, Remodelage et Thrombose (CRT), and Université d'Angers (UA)
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smooth muscle ,Myocytes ,purinoceptor P2Y6 ,[SDV.MHEP.CSC]Life Sciences [q-bio]/Human health and pathology/Cardiology and cardiovascular system ,myosin light chains ,rhoA GTP-binding protein ,nucleotides ,myogenic tone - Abstract
International audience; OBJECTIVE:Myogenic tone (MT) of resistance arteries ensures autoregulation of blood flow in organs and relies on the intrinsic property of smooth muscle to contract in response to stretch. Nucleotides released by mechanical strain on cells are responsible for pleiotropic vascular effects, including vasoconstriction. Here, we evaluated the contribution of extracellular nucleotides to MT.APPROACH AND RESULTS:We measured MT and the associated pathway in mouse mesenteric resistance arteries using arteriography for small arteries and molecular biology. Of the P2 receptors in mouse mesenteric resistance arteries, mRNA expression of P2X1 and P2Y6 was dominant. P2Y6 fully sustained UDP/UTP-induced contraction (abrogated in P2ry6(-/-) arteries). Preventing nucleotide hydrolysis with the ectonucleotidase inhibitor ARL67156 enhanced pressure-induced MT by 20%, whereas P2Y6 receptor blockade blunted MT in mouse mesenteric resistance arteries and human subcutaneous arteries. Despite normal hemodynamic parameters, P2ry6(-/-) mice were protected against MT elevation in myocardial infarction-induced heart failure. Although both P2Y6 and P2Y2 receptors contributed to calcium mobilization, P2Y6 activation was mandatory for RhoA-GTP binding, myosin light chain, P42-P44, and c-Jun N-terminal kinase phosphorylation in arterial smooth muscle cells. In accordance with the opening of a nucleotide conduit in pressurized arteries, MT was altered by hemichannel pharmacological inhibitors and impaired in Cx43(+/-) and P2rx7(-/-) mesenteric resistance arteries.CONCLUSIONS:Signaling through P2 nucleotide receptors contributes to MT. This mechanism encompasses the release of nucleotides coupled to specific autocrine/paracrine activation of the uracil nucleotide P2Y6 receptor and may contribute to impaired tissue perfusion in cardiovascular diseases
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- 2016
38. Blood Thixotropy in Patients with Sickle Cell Anaemia: Role of Haematocrit and Red Blood Cell Rheological Properties
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Vent-Schmidt, Jens, Waltz, Xavier, Romana, Marc, Hardy-Dessources, Marie, Lemonne, Nathalie, Billaud, Marie, Etienne-Julan, Maryse, Connes, Philippe, Lam, Wilbur, Protéines de la membrane érythrocytaire et homologues non-érythroides, Université des Antilles et de la Guyane (UAG)-Institut National de la Transfusion Sanguine [Paris] (INTS)-Université Paris Diderot - Paris 7 (UPD7)-Université de La Réunion (UR)-Institut National de la Santé et de la Recherche Médicale (INSERM), Adaptations au Climat Tropical, Exercice et Santé (ACTES), Université des Antilles et de la Guyane (UAG), Université des Antilles (Pôle Guadeloupe), Université des Antilles (UA), Unité Transversale de la Drépanocytose, CHU Pointe-à-Pitre/Abymes [Guadeloupe] -Hôpital Ricou, Centre de recherche Cardio-Thoracique de Bordeaux [Bordeaux] (CRCTB), Université Bordeaux Segalen - Bordeaux 2-CHU Bordeaux [Bordeaux]-Institut National de la Santé et de la Recherche Médicale (INSERM), CHU Pointe-à-Pitre/Abymes [Guadeloupe], and Hôpital Ricou-CHU Pointe-à-Pitre/Abymes [Guadeloupe]
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[SDV]Life Sciences [q-bio] ,ComputingMilieux_MISCELLANEOUS - Abstract
International audience
- Published
- 2014
39. Proliferative retinopathy and maculopathy are two independent conditions in sickle cell disease: Is there a role of blood rheology?1.
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Beral, Laurence, Lemonne, Nathalie, Romana, Marc, Charlot, Keyne, Billaud, Marie, Acomat, Malik, Zorobabel, Coralie, Nader, Elie, Etienne-Julan, Maryse, David, Thierry, and Connes, Philippe
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SICKLE cell anemia ,HEMORHEOLOGY ,BLOOD viscosity ,HEMATOCRIT - Abstract
OBJECTIVE: Our study investigated the prevalence of retinopathy and maculopathy in sickle cell patients and tested the association between these two conditions. In addition, we tested whether hematological and hemorheological parameters, as well as genotype, were involved in the development of these two conditions. METHODS: Seventy sickle cell adult patients were recruited: 37 with sickle cell anemia (SCA) and 33 with sickle cell hemoglobin C disease (SCC). All patients underwent retinal examination and macular ocular coherence tomography. Blood was sampled for the measurements of hematological and hemorheological parameters. RESULTS: Twenty-six patients had maculopathy and 30 had retinopathy with no significant difference between SCA and SCC patients. No association between the presence of retinopathy and maculopathy was detected. RBC aggregation was higher and RBC deformability lower at 3 Pa in SCA patients. Blood viscosity and hematocrit were higher in SCC than in SCA patients. However, no association was found between biological parameters and the ocular complications studied. CONCLUSIONS: Our study showed that retinopathy and maculopathy are common in sickle cell disease. Nevertheless, we found no association with hematological parameters, blood rheology or genotype. [ABSTRACT FROM AUTHOR]
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- 2019
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40. Measuring workload with electrodermal activity during common braking actions
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Messonnier, Laurent A., Chatel, Benjamin, Messonnier, Laurent, Barge, Quentin, Vilmen, Christophe, Noirez, Philippe, Bernard, Monique, Pialoux, Vincent, Bendahan, David, Brudey, Laura, Cita, Kizzy-Clara, Brureau, Laurent, Lemonne, Nathalie, Billaud, Marie, Connes, Philippe, Ferdinand, Séverine, Tressieres, Benoit, Tarer, Vanessa, Etienne-Julan, Maryse, Blanchet, Pascal, Elion, Jacques, Romana, Marc, Lam, Wilbur, Collet, C., Salvia, E., Petit-Boulanger, C., Centre de résonance magnétique biologique et médicale (CRMBM), Aix Marseille Université (AMU)-Assistance Publique - Hôpitaux de Marseille (APHM)-Centre National de la Recherche Scientifique (CNRS), Laboratory of Exercise Physiology, University of Savoie, Chambery, and University Jean Monnet of Saint-Etienne, Saint-Etienne, Laboratory of Exercise Physiology, Institut national du sport, de l'expertise et de la performance (INSEP), Laboratoire de Physiologie-Biologie du Sport, Université d'Auvergne - Clermont-Ferrand I (UdA), Observatoire Régional de la Santé de la Guadeloupe, Institut de recherche en santé, environnement et travail (Irset), Université d'Angers (UA)-Université de Rennes 1 (UR1), Université de Rennes (UNIV-RENNES)-Université de Rennes (UNIV-RENNES)-École des Hautes Études en Santé Publique [EHESP] (EHESP)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Structure Fédérative de Recherche en Biologie et Santé de Rennes ( Biosit : Biologie - Santé - Innovation Technologique ), Unité Transversale de la Drépanocytose [Pointe-à-Pitre, Guadeloupe], CHU Pointe-à-Pitre/Abymes [Guadeloupe], Centre de recherche Cardio-Thoracique de Bordeaux [Bordeaux] (CRCTB), Université Bordeaux Segalen - Bordeaux 2-CHU Bordeaux [Bordeaux]-Institut National de la Santé et de la Recherche Médicale (INSERM), Laboratoire Interuniversitaire de Biologie de la Motricité (LIBM ), Université Claude Bernard Lyon 1 (UCBL), Université de Lyon-Université de Lyon-Université Jean Monnet [Saint-Étienne] (UJM)-Université Savoie Mont Blanc (USMB [Université de Savoie] [Université de Chambéry]), Centre d'investigation clinique Antilles-Guyane (CIC - Antilles Guyane), Institut National de la Santé et de la Recherche Médicale (INSERM)-CHU Pointe-à-Pitre/Abymes [Guadeloupe] -CHU de la Martinique [Fort de France]-Centre Hospitalier Andrée Rosemon [Cayenne, Guyane Française], Service de Neurologie [CHU Pointe à Pitre], Insern, UMR 763, Hôpital Robert Debré, Université Paris Diderot - Paris 7 (UPD7), Pharmacogénétique et abords thérapeutiques des maladies héréditaires, Université des Antilles et de la Guyane (UAG)-Université Paris Diderot - Paris 7 (UPD7)-IFR2-Institut National de la Santé et de la Recherche Médicale (INSERM), Hôpital Lariboisière, Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Hôpital Lariboisière-Fernand-Widal [APHP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Université Paris Diderot - Paris 7 (UPD7), Institut National de la Santé et de la Recherche Médicale (INSERM)-CHU de la Martinique [Fort de France]-CHU Pointe-à-Pitre/Abymes [Guadeloupe] -Centre Hospitalier Andrée Rosemon [Cayenne, Guyane Française], Assistance publique - Hôpitaux de Paris (AP-HP) (APHP)-Hôpital Lariboisière-Université Paris Diderot - Paris 7 (UPD7), Laboratoire de Physiologie de l'Exercice (LPE), Université Jean Monnet - Saint-Étienne (UJM), Université d'Angers (UA)-Université de Rennes (UR)-École des Hautes Études en Santé Publique [EHESP] (EHESP)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Structure Fédérative de Recherche en Biologie et Santé de Rennes ( Biosit : Biologie - Santé - Innovation Technologique ), and Université de Lyon-Université de Lyon-Université Jean Monnet - Saint-Étienne (UJM)-Université Savoie Mont Blanc (USMB [Université de Savoie] [Université de Chambéry])
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Adult ,medicine.medical_specialty ,Automobile Driving ,[SDV]Life Sciences [q-bio] ,Physical Therapy, Sports Therapy and Rehabilitation ,Human Factors and Ergonomics ,Workload ,Galvanic Skin Response ,Audiology ,Middle Aged ,Young Adult ,Mental condition ,Electrodermal response ,medicine ,Humans ,[SDV.NEU]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC] ,Mental load ,Emergencies ,Skin conductance ,Psychology ,Simulation ,Stress, Psychological ,ComputingMilieux_MISCELLANEOUS - Abstract
How to assess mental load remains a recurrent question. We aimed to explore whether slight differences in real-world driving task demands could be discriminated by electrodermal response (EDR). A sample of 33 participants was observed under five conditions: controlled braking from 50 to 30 km/h, 80 to 50 km/h, 50 to 0 km/h, 80 to 0 km/h, and a single unexpected emergency braking event from 80 to 0 km/h. The likelihood of EDR and, whenever present, its duration were both correlated with workload as represented by the deceleration demand. A higher base travel speed and the unexpected demand of the emergency braking situation impacted EDR, thus attesting higher workload level. EDR explains why stopping the vehicle from 50 km/h and slowing down from 80 to 50 km/h was of similar strain. The results further demonstrate that EDR measures can be successfully employed to discriminate multiple levels of workload.Common braking elicited different loads as revealed by electrodermal response (EDR) with sensitivity to deceleration of - 0.2 g. Even the slightest braking elicited a strain measurable with EDR. Accordingly, EDR may objectively assess the resulting strain during driving, with enhanced reliability if associated with other variables, e.g. cardiac activity.
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- 2014
41. Klf4 has an unexpected protective role in perivascular cells within the microvasculature.
- Author
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Haskins, Ryan M., Nguyen, Anh T., Alencar, Gabriel F., Billaud, Marie, Kelly-Goss, Molly R., Good, Miranda E., Bottermann, Katharina, Klibanov, Alexander L., French, Brent A., Harris, Thurl E., Peirce, Shayn M., Isakson, Brant E., and Owens, Gary K.
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KRUPPEL-like factors ,VASCULAR smooth muscle ,ATHEROSCLEROSIS - Abstract
Recent smooth muscle cell (SMC) lineage-tracing studies have revealed that SMCs undergo remarkable changes in phenotype during development of atherosclerosis. Of major interest, we demonstrated that Kruppel-like factor 4 (KLF4) in SMCs is detrimental for overall lesion pathogenesis, in that SMC-specific conditional knockout of the KLF4 gene (Klf4) resulted in smaller, more-stable lesions that exhibited marked reductions in the numbers of SMC-derived macrophage- and mesenchymal stem cell-like cells. However, since the clinical consequences of atherosclerosis typically occur well after our reproductive years, we sought to identify beneficial KLF4-dependent SMC functions that were likely to be evolutionarily conserved. We tested the hypothesis that KLF4-dependent SMC transitions play an important role in the tissue injury-repair process. Using SMC-specific lineage-tracing mice positive and negative for simultaneous SMC-specific conditional knockout of Klf4, we demonstrate that SMCs in the remodeling heart after ischemia-reperfusion injury (IRI) express KLF4 and transition to a KLF4-dependent macrophage-like state and a KLF4-independent myofibroblast-like state. Moreover, heart failure after IRI was exacerbated in SMC Klf4 knockout mice. Surprisingly, we observed a significant cardiac dilation in SMC Klf4 knockout mice before IRI as well as a reduction in peripheral resistance. KLF4 chromatin immunoprecipitation- sequencing analysis on mesenteric vascular beds identified potential baseline SMC KLF4 target genes in numerous pathways, including PDGF and FGF. Moreover, microvascular tissue beds in SMC Klf4 knockout mice had gaps in lineage-traced SMC coverage along the resistance arteries and exhibited increased permeability. Together, these results provide novel evidence that Klf4 has a critical maintenance role within microvascular SMCs: it is required for normal SMC function and coverage of resistance arteries. [ABSTRACT FROM AUTHOR]
- Published
- 2018
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42. Bicuspid Aortic Valve Morphotype Correlates With Regional Antioxidant Gene Expression Profiles in the Proximal Ascending Aorta.
- Author
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Phillippi, Julie A., Hill, Jennifer C., Billaud, Marie, Green, Benjamin R., Kotlarczyk, Mary P., and Gleason, Thomas G.
- Abstract
Background Bicuspid aortic valve (BAV) is associated with asymmetric dilatation of the proximal ascending aorta. We previously demonstrated increased susceptibility of smooth muscle cells to oxidative stress in the BAV-aneurysmal aorta and hypothesized that antioxidant expression is regionally defined and influenced by the BAV morphotype. Methods BAV valve morphology was defined according to number of raphes: type 0 (0 raphes), type 1 (1 raphe), or type 2 (2 raphes) and by the raphe location among the left (L), right (R) or non (N) coronary cusps. Ascending aortic specimens were partitioned into three regions corresponding to the sinuses of Valsalva, denoted R, N (greater curve), and L (lesser curve). Transcripts 1, 2, and 3 from the gene expressing superoxide dismutase ( Sod ) were quantified in all three regions. Results were compared with aneurysmal and nonaneurysmal aortic specimens from patients with a tricuspid aortic valve. Results Region-specific Sod1 upregulation and Sod2 downregulation were dependent on the BAV morphotype. Sod3 was uniformly downregulated in all regions in a morphotype-independent manner. Sod1 upregulation was noted in the R region of the nonaneurysmal type 1 L/R morphotype. Aortic valve regurgitation, but not stenosis, affected the expression of Sod isoforms in specimens of degenerative aneurysms. Conclusions Region-specific transcription profiles of Sod on the basis of BAV morphotype deepen our understanding of its associated aortopathy and provide biological insight on the asymmetric dilatation pattern. This work indicates regional differences exist in the oxidative stress biology of the proximal aortic wall, and this may lead to newer diagnostic techniques to adjudicate aortic catastrophe risk. [ABSTRACT FROM AUTHOR]
- Published
- 2017
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43. Signaling Pathways Linked to Serotonin-Induced Superoxide Anion Production: A Physiological Role for Mitochondria in Pulmonary Arteries.
- Author
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Genet, Nafiisha, Billaud, Marie, Rossignol, Rodrigue, Dubois, Mathilde, Gillibert-Duplantier, Jennifer, Isakson, Brant E., Marthan, Roger, Savineau, Jean-Pierre, and Guibert, Christelle
- Subjects
SEROTONIN ,SUPEROXIDES ,PULMONARY artery ,MITOCHONDRIA ,JAK-STAT pathway - Abstract
Serotonin (5-HT) is a potent vasoconstrictor agonist and contributes to several vascular diseases including systemic or pulmonary hypertension and atherosclerosis. Although superoxide anion (O
2 •- ) is commonly associated to cellular damages due to O2 •- overproduction, we previously demonstrated that, in physiological conditions, O2 •- also participates to the 5-HT contraction in intrapulmonary arteries (IPA). Here, we focused on the signaling pathways leading to O2 •- production in response to 5-HT in rat IPA. Using electron paramagnetic resonance on rat IPA, we showed that 5-HT (100μM)-induced O2 •- production was inhibited by ketanserin (1μM-an inhibitor of the 5-HT2 receptor), absence of extracellular calcium, two blockers of voltage-independent calcium permeable channels (RHC80267 50μM and LOE-908 10μM) and a blocker of the mitochondrial complex I (rotenone-100 nM). Depletion of calcium from the sarcoplasmic reticulum or nicardipine (1μM-an inhibitor of the L-type voltage-dependent calcium channel) had no effect on the 5-HT-induced O2 •- production. O2 •- levels were also increased by a-methyl-5-HT (10μM-a 5-HT2 receptors agonist) whereas GR127935 (1μM-an antagonist of the 5-HT 1B/D receptor) and citalopram (1μM-a 5-HT transporter inhibitor) had no effect on the 5-HT-induced O2 •- production. Peroxynitrites were increased in response to 5-HT (100μM). In isolated pulmonary arterial smooth muscle cells loaded with rhod-2 or mitosox probes, we respectively showed that 5-HT increased both mitochondrial calcium and O2 •- levels, which were both abrogated in absence of extracellular calcium. Mitochondrial O2 •- levels were also abolished in the presence of rotenone (100 nM). In pulmonary arterial smooth muscle cells loaded with TMRM, we showed that 5-HT transiently depolarized the mitochondrial membrane whereas in the absence of extracellular calcium the mitochondrial membrane depolarisation was delayed and sustained in response to 5-HT. 5-HT decreased the mitochondrial respiratory rate measured with a Clark oxygen electrode. Altogether, in physiological conditions, 5-HT acts on 5-HT2 receptors and induces an O2 •- production dependent on extracellular calcium and mitochondria. [ABSTRACT FROM AUTHOR]- Published
- 2017
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44. Regional Disruptions in Endothelial Nitric Oxide Pathway Associated With Bicuspid Aortic Valve.
- Author
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Kotlarczyk, Mary P., Billaud, Marie, Green, Benjamin R., Hill, Jennifer C., Shiva, Sruti, Kelley, Eric E., Phillippi, Julie A., and Gleason, Thomas G.
- Abstract
Background Endothelial nitric oxide (NO) synthase (eNOS) has been implicated in the development of bicuspid aortic valve (BAV) and with differential expression in the ascending aorta of BAV patients. However, little is known about functional disruptions in the eNOS pathway and the effect on BAV-associated aortic dilatation. We tested the hypothesis that eNOS function is regionally diminished in ascending thoracic aortic aneurysms associated with BAV. Methods Thoracic aortic aneurysms specimens were collected from patients with BAV (n = 21) or tricuspid aortic valve (n = 12). Tissue samples were harvested from three circumferential regions corresponding to locations above the right, left, and noncoronary sinuses. Adventitial-stripped specimens containing media and intima only were analyzed for NO synthase 3 gene expression and total eNOS protein. Indicators of eNOS activity (pSer1177-eNOS) and NO bioavailability (phosphorylation of vasodilator-stimulated phosphoprotein at Ser239) were also measured. Results NO synthase 3 and eNOS protein were elevated in the right aortic region of BAV specimens compared with tricuspid aortic valve specimens. Activation of eNOS, as indicated by pSer1177-eNOS, was higher in BAV specimens across all regions. Despite increases in eNOS and pSer1177-eNOS, BAV specimens displayed no change in pSer239-vasodilator-stimulated phosphoprotein compared with tricuspid aortic valve specimens. Conclusions BAV is associated with regional disruptions in the eNOS pathway, most markedly in the right aortic region. The discrepancy between increased eNOS activity and the absence of increased NO bioavailability in this region provides insight into physiologic mechanisms potentially underlying the asymmetric dilatation pattern observed in BAV. [ABSTRACT FROM AUTHOR]
- Published
- 2016
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45. Central Role of P2Y6 UDP Receptor in Arteriolar Myogenic Tone.
- Author
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Kauffenstein, Gilles, Tamareille, Sophie, Prunier, Fabrice, Roy, Charlotte, Ayer, Audrey, Toutain, Bertrand, Billaud, Marie, Isakson, Brant E., Grimaud, Linda, Loufrani, Laurent, Rousseau, Pascal, Abraham, Pierre, Procaccio, Vincent, Monyer, Hannah, de Wit, Cor, Boeynaems, Jean-Marie, Robaye, Bernard, Kwak, Brenda R., and Henrion, Daniel
- Published
- 2016
- Full Text
- View/download PDF
46. Men with Sickle Cell Anemia and Priapism Exhibit Increased Hemolytic Rate, Decreased Red Blood Cell Deformability and Increased Red Blood Cell Aggregate Strength.
- Author
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Cita, Kizzy-Clara, Brureau, Laurent, Lemonne, Nathalie, Billaud, Marie, Connes, Philippe, Ferdinand, Séverine, Tressières, Benoit, Tarer, Vanessa, Etienne-Julan, Maryse, Blanchet, Pascal, Elion, Jacques, and Romana, Marc
- Subjects
SICKLE cell anemia ,PRIAPISM ,HEMOLYTIC anemia ,DISEASES in men ,ERYTHROCYTE deformability ,BIOLOGICAL aggregation ,HEMORHEOLOGY ,OPTICAL rotation - Abstract
Objectives: To investigate the association between priapism in men with sickle cell anemia (SCA) and hemorheological and hemolytical parameters. Materials and Methods: Fifty-eight men with SCA (median age: 38 years) were included; 28 who had experienced priapism at least once during their life (priapism group) and 30 who never experienced this complication (control group). Twenty-two patients were treated with hydroxycarbamide, 11 in each group. All patients were at steady state at the time of inclusion. Hematological and biochemical parameters were obtained through routine procedures. The Laser-assisted Optical Rotational Cell Analyzer was used to measure red blood cell (RBC) deformability at 30 Pa (ektacytometry) and RBC aggregation properties (laser backscatter versus time). Blood viscosity was measured at a shear rate of 225 s
-1 using a cone/plate viscometer. A principal component analysis was performed on 4 hemolytic markers (i.e., lactate dehydrogenase (LDH), aspartate aminotransferase (ASAT), total bilirubin (BIL) levels and reticulocyte (RET) percentage) to calculate a hemolytic index. Results: Compared to the control group, patients with priapism exhibited higher ASAT (p = 0.01), LDH (p = 0.03), RET (p = 0.03) levels and hemolytic indices (p = 0.02). Higher RBC aggregates strength (p = 0.01) and lower RBC deformability (p = 0.005) were observed in patients with priapism compared to controls. After removing the hydroxycarbamide-treated patients, RBC deformability (p = 0.01) and RBC aggregate strength (p = 0.03) were still different between the two groups, and patients with priapism exhibited significantly higher hemolytic indices (p = 0.01) than controls. Conclusion: Our results confirm that priapism in SCA is associated with higher hemolytic rates and show for the first time that this complication is also associated with higher RBC aggregate strength and lower RBC deformability. [ABSTRACT FROM AUTHOR]- Published
- 2016
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47. Pfaffia paniculata extract improves red blood cell deformability in sickle cell patients.
- Author
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Mozar, Anais, Charlot, Keyne, Sandor, Barbara, Rabaï, Miklos, Lemonne, Nathalie, Billaud, Marie, Hardy-Dessources, Marie-Dominique, Beltan, Eric, Pandey, Ramesh C., Connes, Philippe, and Ballas, Samir K.
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PFAFFIAN systems ,BLOOD cell physiology ,SICKLE cell anemia ,ERYTHROCYTES ,HEMOGLOBINS ,PATIENTS - Abstract
The aim of the present study was to test the effects of Pfaffia paniculata (PP) extract on the red blood cell (RBC) rheological properties of patients with sickle cell disease (SCD) and healthy (AA) individuals. Blood from 7 SCD and 4 AA individuals were collected in EDTA tubes. Washed RBCs were incubated with various concentration of PP extract: 0.0, 0.2 or 0.5 mg/ml of PP solution for 5 hrs at 37°C. RBC deformability was measured by ektacytometry at 9 shear stresses ranging from 0.3 to 30 Pa, and RBC aggregation properties were determined by laser-backscattered techniques. Because RBCs from SCD patients are fragile, a stability test was also performed to test for the fragility of RBC exposed to a constant shear stress (70 Pa) for 10 min. While RBC deformability was not improved by the use of PP extract in AA, we noted an improvement of this parameter in patients with SCD between the 0.0 and 0.5 mg/ml conditions. In contrast to AA RBCs, the fragility of SCD RBCs was not affected by PP extract. In conclusion, this study demonstrates the beneficial effects, in-vitro, of PP extract on the RBC deformability of SCD patients, notably at high shear stress (a shear stress condition usually found in capillaries). [ABSTRACT FROM AUTHOR]
- Published
- 2016
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48. Rheology of red blood cells in patients with HbC disease.
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Lemonne, Nathalie, Billaud, Marie, Waltz, Xavier, Romana, Marc, Hierso, R´egine, Etienne-Julan, Maryse, and Connes, Philippe
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ERYTHROCYTES , *BLOOD hyperviscosity syndrome , *BLOOD viscosity , *PATIENT management ,HEALTH management - Abstract
Patients with hemoglobin C disease (CC) usually do not develop severe complications in comparison with individuals with sickle cell anemia (SS) or with sickle cell hemoglobin C disease (SC). The present study compared the hematological, biochemical, hemorheological and clinical characteristics of CC patients to those of SS, SC and healthy individuals (AA). Blood viscosity was measured at 225 s-1 with a cone plate viscometer. The hematocrit-to-blood viscosity ratio (HVR), i.e. an index of red blood cell (RBC) oxygen transport effectiveness, was calculated. RBC deformability was determined at 30 Pa by ektacytometry, and RBC aggregation properties by syllectometry. CC and SC had higher blood viscosity and lower HVR than AA. Nevertheless, HVR was higher in CC compared to SS and tended to be higher than in SC. The CC group exhibited very rigid hyperchromic RBC compared to the three other groups. RBC aggregation abnormalities were observed in CC: low RBC aggregation index and high RBC aggregates strength. Despite these hemorheological abnormalities, CC never had hospitalized painful vaso-occlusive crisis or acute chest syndrome. In contrast, all of them had splenomegaly.Of note, 2 out of 7 CC developed retinopathy or otologic disorders. Whether the blood hyperviscosity and decreased RBC deformability are responsible for these complications is unknown. The higher oxygen transport effectiveness (i.e., HVR) of CC compared to SS is probably at the origin of the very low risk of medical complication in this population. [ABSTRACT FROM AUTHOR]
- Published
- 2015
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49. Emerging concepts regarding pannexin 1 in the vasculature.
- Author
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Good, Miranda E., Begandt, Daniela, DeLalio, Leon J., Keller, Alexander S., Billaud, Marie, and Isakson, Brant E.
- Subjects
PANNEXINS ,BLOOD vessels ,ION channels ,ADENOSINE triphosphate ,CELLULAR signal transduction ,RNA interference - Abstract
Pannexin channels are newly discovered ATP release channels expressed throughout the body. Pannexin 1 (Panx1) channels have become of great interest as they appear to participate in a multitude of signalling cascades, including regulation of vascular function. Although numerous Panx1 pharmacological inhibitors have been discovered, these inhibitors are not specific for Panx1 and have additional effects on other proteins. Therefore, molecular tools, such as RNA interference and knockout animals, are needed to demonstrate the role of pannexins in various cellular functions. This review focuses on the known roles of Panx1 related to purinergic signalling in the vasculature focusing on post-translational modifications and channel gating mechanisms that may participate in the regulated release of ATP. [ABSTRACT FROM AUTHOR]
- Published
- 2015
- Full Text
- View/download PDF
50. A molecular signature in the pannexin1 intracellular loop confers channel activation by the a1 adrenoreceptor in smooth muscle cells.
- Author
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Parpaite, Thibaud, Butcher, Joshua T., Mutchler, Stephanie M., Best, Angela K., Billaud, Marie, Lohman, Alexander W., DeLalio, Leon J., Somlyo, Avril V., Isakson, Brant E., Artamonov, Mykhaylo V., Yu-Hsin Chiu, Sandilos, Joanna K., Bayliss, Douglas A., Thompson, Roger J., Le, Thu H., and Ravichandran, Kodi S.
- Published
- 2015
- Full Text
- View/download PDF
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