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4. Androgenic steroids induce pathologic scarring in a preclinical porcine model via dysfunctional extracellular matrix deposition

Author

Reiche, Erik, primary, Keller, Patrick R., additional, Soares, Vance, additional, Schuster, Calvin R., additional, Rahmayanti, Siti, additional, Mroueh, Jessica, additional, Mroueh, Vanessa, additional, Billaud, Marie, additional, Hu, Sophia, additional, Hoover‐Watson, Hunter, additional, Lian, Christine G., additional, Tan, Yu, additional, Doloff, Joshua C., additional, Newell‐Fugate, Annie E., additional, and Coon, Devin, additional

Published
2024
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5. Only the strong "aorta" survives: the female edge in a mouse model of severe Marfan syndrome.

Author

Billaud, Marie and Phillippi, Julie A.

Subjects
*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]

Published
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.

Author

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

Subjects
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]

Published
2024
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9. Androgenic Steroids Induce Pathologic Scarring in a Preclinical Swine Model Via Dysfunctional Extracellular Matrix Deposition

Author

Reiche, Erik, primary, Keller, Patrick R, additional, Soares, Vance, additional, Schuster, Calvin R, additional, Billaud, Marie, additional, Rahmayanti, Siti, additional, Hu, Sophia, additional, Hover-Watson, Hunter, additional, Mroueh, Jessica, additional, Mroueh, Vanessa, additional, Tan, Yu, additional, Kim, Seo Young, additional, Newell-Fugate, Annie E, additional, Lian, Christine G, additional, and Coon, Devin, additional

Published
2023
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10. Abstract 100: Multi-omics And Single Nucleus Transcriptomics Reveal Aberrant Adaptive Immune Responses In Human Bicuspid Aortic Valves

Author

Blaser, Mark C, primary, Reichart, Daniel, additional, Sonawane, Abhijeet, additional, Schlotter, Florian, additional, Halu, Arda, additional, Passos, Livia Silva A, additional, DeLaughter, Daniel, additional, Zhou, Wunan, additional, Blankstein, Ron, additional, DI CARLI, MARCELO, additional, Nunes, Maria D, additional, Billaud, Marie, additional, Sabe, Ashraf A, additional, Robson, Simon, additional, Body, Simon C, additional, Muehlschlegel, Jochen D, additional, Seidman, Jonathan G, additional, Seidman, Christine E, additional, Aikawa, Masanori, additional, Singh, Sasha A, additional, and Aikawa, Elena, additional

Published
2023
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14. Aortic Dissection is Determined by Specific Shape and Hemodynamic Interactions

Author

Massachusetts Institute of Technology. Institute for Medical Engineering & Science, Williams, Jessica G., Marlevi, David, Bruse, Jan L., Nezami, Farhad R., Moradi, Hamed, Fortunato, Ronald N., Maiti, Spandan, Billaud, Marie, Edelman, Elazer R., Gleason, Thomas G., Massachusetts Institute of Technology. Institute for Medical Engineering & Science, 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.

Abstract

The aim of this study was to determine whether specific three-dimensional aortic shape features, extracted via statistical shape analysis (SSA), correlate with the development of thoracic ascending aortic dissection (TAAD) risk and associated aortic hemodynamics. Thirty-one patients followed prospectively with ascending thoracic aortic aneurysm (ATAA), who either did (12 patients) or did not (19 patients) develop TAAD, were included in the study, with aortic arch geometries extracted from computed tomographic angiography (CTA) imaging. Arch geometries were analyzed with SSA, and unsupervised and supervised (linked to dissection outcome) shape features were extracted with principal component analysis (PCA) and partial least squares discriminant analysis (PLS-DA), respectively. We determined PLS-DA to be effective at separating dissection and no-dissection patients ( $$p = 0.0010$$ p = 0.0010 ), with decreased tortuosity and more equal ascending and descending aortic diameters associated with higher dissection risk. In contrast, neither PCA nor traditional morphometric parameters (maximum diameter, tortuosity, or arch volume) were effective at separating dissection and no-dissection patients. The arch shapes associated with higher dissection probability were supported with hemodynamic insight. Computational fluid dynamics (CFD) simulations revealed a correlation between the PLS-DA shape features and wall shear stress (WSS), with higher maximum WSS in the ascending aorta associated with increased risk of dissection occurrence. Our work highlights the potential importance of incorporating higher dimensional geometric assessment of aortic arch anatomy in TAAD risk assessment, and in considering the interdependent influences of arch shape and hemodynamics as mechanistic contributors to TAAD occurrence.

Published
2023

16. Non-canonical Telomerase Reverse Transcriptase Controls Osteogenic Differentiation of Aortic Valve Cells Through STAT5

Author

Cuevas, Rolando A., primary, Hortells, Luis, additional, Chu, Claire C., additional, Wong, Ryan, additional, Crane, Alex, additional, Boufford, Camille, additional, Regan, Cailyn, additional, Moorhead, William J., additional, Bashline, Michael J., additional, Parwal, Aneesha, additional, Parise, Angelina M., additional, Gurkar, Aditi, additional, Bruemmer, Dennis, additional, Sembrat, John, additional, Sultan, Ibrahim, additional, Gleason, Thomas G., additional, Billaud, Marie, additional, and St. Hilaire, Cynthia, additional

Published
2022
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18. Adventitia-derived extracellular matrix hydrogel enhances contractility of human vasa vasorum-derived pericytes via α(2)β(1) integrin and TGFβ receptor

Author

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.

Subjects
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.

Published
2022

19. Adventitia‐derived extracellular matrix hydrogel enhances contractility of human vasa vasorum‐derived pericytes via α 2 β 1 integrin and TGFβ receptor

Author

Wintruba, Kaitlyn L., primary, Hill, Jennifer C., additional, Richards, Tara D., additional, Lee, Yoojin C., additional, Kaczorowski, David J., additional, Sultan, Ibrahim, additional, Badylak, Stephen F., additional, Billaud, Marie, additional, Gleason, Thomas G., additional, and Phillippi, Julie A., additional

Published
2022
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25. Adventitia‐derived extracellular matrix hydrogel enhances contractility of human vasa vasorum‐derived pericytes via α2β1 integrin and TGFβ receptor.

Author

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]

Published
2022
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26. Contributors

Author

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

Published
2024
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27. Abstract MP08: Telomerase Reverse Transcriptase Mediates Osteogenesis In Calcific Aortic Valve Disease

Author

Cuevas, Rolando A, primary, Hortells, Luis, additional, Boufford, Camille, additional, Regan, Cailyn, additional, Wong, Ryan, additional, Crane, Alexander, additional, Chu, Claire, additional, Moorhead, William, additional, Lee, Angela, additional, Bashline, Michael, additional, Gurkar, Aditi, additional, Bruemmer, Dennis, additional, rojas, mauricio, additional, Gleason, Thomas G, additional, Billaud, Marie, additional, Sultan, Ibrahim, additional, and St Hilaire, Cynthia, additional

Published
2021
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31. Common deletion variants causing protocadherin-α deficiency contribute to the complex genetics of BAV and left-sided congenital heart disease

Author

Teekakirikul, Polakit, primary, Zhu, Wenjuan, additional, Gabriel, George C., additional, Young, Cullen B., additional, Williams, Kylia, additional, Martin, Lisa J., additional, Hill, Jennifer C., additional, Richards, Tara, additional, Billaud, Marie, additional, Phillippi, Julie A., additional, Wang, Jianbin, additional, Wu, Yijen, additional, Tan, Tuantuan, additional, Devine, William, additional, Lin, Jiuann-huey, additional, Bais, Abha S., additional, Klonowski, Jonathan, additional, de Bellaing, Anne Moreau, additional, Saini, Ankur, additional, Wang, Michael X., additional, Emerel, Leonid, additional, Salamacha, Nathan, additional, Wyman, Samuel K., additional, Lee, Carrie, additional, Li, Hung Sing, additional, Miron, Anastasia, additional, Zhang, Jingyu, additional, Xing, Jianhua, additional, McNamara, Dennis M., additional, Fung, Erik, additional, Kirshbom, Paul, additional, Mahle, William, additional, Kochilas, Lazaros K., additional, He, Yihua, additional, Garg, Vidu, additional, White, Peter, additional, McBride, Kim L., additional, Benson, D. Woodrow, additional, Gleason, Thomas G., additional, Mital, Seema, additional, and Lo, Cecilia W., additional

Published
2021
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38. Oxidative stress, inflammation, blood rheology, and microcirculation in adults with sickle cell disease: Effects of hydroxyurea treatment and impact of sickle cell syndrome

Author

Connes, Philippe, primary, Möckesch, Berenike, additional, Tudor Ngo Sock, Emilienne, additional, Hardy‐Dessources, Marie‐Dominique, additional, Reminy, Karen, additional, Skinner, Sarah, additional, Billaud, Marie, additional, Nader, Elie, additional, Tressieres, Benoit, additional, Etienne‐Julan, Maryse, additional, Guillot, Nicolas, additional, Lemonne, Nathalie, additional, Hue, Olivier, additional, Romana, Marc, additional, and Antoine‐Jonville, Sophie, additional

Published
2021
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43. Posttranslational Modifications in Connexins and Pannexins

Author

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

Published
2018

44. Proliferative retinopathy and maculopathy are two independent conditions in sickle cell disease: Is there a role of blood rheology?1

Author

Beral, Laurence, primary, Lemonne, Nathalie, additional, Romana, Marc, additional, Charlot, Keyne, additional, Billaud, Marie, additional, Acomat, Malik, additional, Zorobabel, Coralie, additional, Nader, Elie, additional, Etienne-Julan, Maryse, additional, David, Thierry, additional, and Connes, Philippe, additional

Published
2019
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45. Constitutive SRC-mediated phosphorylation of pannexin 1 at tyrosine 198 occurs at the plasma membrane

Author

DeLalio, Leon J., primary, Billaud, Marie, additional, Ruddiman, Claire A., additional, Johnstone, Scott R., additional, Butcher, Joshua T., additional, Wolpe, Abigail G., additional, Jin, Xueyao, additional, Keller, T.C. Stevenson, additional, Keller, Alexander S., additional, Rivière, Thibaud, additional, Good, Miranda E., additional, Best, Angela K., additional, Lohman, Alexander W., additional, Swayne, Leigh Anne, additional, Penuela, Silvia, additional, Thompson, Roger J., additional, Lampe, Paul D., additional, Yeager, Mark, additional, and Isakson, Brant E., additional

Published
2019
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46. Role of the gap junctions in the contractile response to agonists in pulmonary artery from two rat models of pulmonary hypertension

Author

Dahan Diana, Billaud Marie, Marthan Roger, Savineau Jean-Pierre, and Guibert Christelle

Subjects
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.

Published
2011
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48. Klf4 has an unexpected protective role in perivascular cells within the microvasculature

Author

Haskins, Ryan M., primary, Nguyen, Anh T., additional, Alencar, Gabriel F., additional, Billaud, Marie, additional, Kelly-Goss, Molly R., additional, Good, Miranda E., additional, Bottermann, Katharina, additional, Klibanov, Alexander L., additional, French, Brent A., additional, Harris, Thurl E., additional, Peirce, Shayn M., additional, Isakson, Brant E., additional, and Owens, Gary K., additional

Published
2018
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49. Classification and Functional Characterization of Vasa Vasorum-Associated Perivascular Progenitor Cells in Human Aorta

Author

Billaud, Marie, Donnenberg, Vera S., Ellis, Bradley W., Meyer, E. Michael, Donnenberg, Albert D., Hill, Jennifer C., Richards, Tara D., Gleason, Thomas G., Phillippi, Julie A., Billaud, Marie, Donnenberg, Vera S., Ellis, Bradley W., Meyer, E. Michael, Donnenberg, Albert D., Hill, Jennifer C., Richards, Tara D., Gleason, Thomas G., and Phillippi, Julie A.

Abstract

In the microcirculation, pericytes are believed to function as mesenchymal stromal cells (MSCs). We hypothesized that the vasa vasorum harbor progenitor cells within the adventitia of human aorta. Pericytes, endothelial progenitor cells, and other cell subpopulations were detected among freshly isolated adventitial cells using flow cytometry. Purified cultured pericytes were enriched for the MSC markers CD105 and CD73 and depleted of the endothelial markers von Willebrand factor and CD31. Cultured pericytes were capable of smooth muscle lineage progression including inducible expression of smooth muscle myosin heavy chain, calponin, and α-smooth muscle actin, and adopted a spindle shape. Pericytes formed spheroids when cultured on Matrigel substrates and peripherally localized with branching endothelial cells in vitro. Our results indicate that the vasa vasorum form a progenitor cell niche distinct from other previously described progenitor populations in human adventitia. These findings could have important implications for understanding the complex pathophysiology of human aortic disease.

Published
2017

50. Mechanisms of ATP release and signalling in the blood vessel wall

Author

Lohman, Alexander W., Billaud, Marie, Isakson, Brant E., Lohman, Alexander W., Billaud, Marie, and Isakson, Brant E.

Abstract

The nucleotide adenosine 5′-triphosphate (ATP) has classically been considered the cell's primary energy currency. Importantly, a novel role for ATP as an extracellular autocrine and/or paracrine signalling molecule has evolved over the past century and extensive work has been conducted to characterize the ATP-sensitive purinergic receptors expressed on almost all cell types in the body. Extracellular ATP elicits potent effects on vascular cells to regulate blood vessel tone but can also be involved in vascular pathologies such as atherosclerosis. While the effects of purinergic signalling in the vasculature have been well documented, the mechanism(s) mediating the regulated release of ATP from cells in the blood vessel wall and circulation are now a key target of investigation. The aim of this review is to examine the current proposed mechanisms of ATP release from vascular cells, with a special emphasis on the transporters and channels involved in ATP release from vascular smooth muscle cells, endothelial cells, circulating red blood cells, and perivascular sympathetic nerves, including vesicular exocytosis, plasma membrane F1/F0-ATP synthase, ATP-binding cassette (ABC) transporters, connexin hemichannels, and pannexin channels

Published
2017

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