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1. Hyperacute pathophysiology of traumatic and vascular brain injury captured by ultrasound, photoacoustic, and magnetic resonance imaging

Author

Kamali, Ali, Dieckhaus, Laurel, Peters, Emily C., Preszler, Collin A., Witte, Russel S., Pires, Paulo W., Hutchinson, Elizabeth B., and Laksari, Kaveh

Subjects
Quantitative Biology - Quantitative Methods, Quantitative Biology - Tissues and Organs
Abstract

Cerebrovascular dynamics and pathomechanisms that evolve in the minutes and hours following traumatic vascular injury in the brain remain largely unknown. We investigated the pathophysiology evolution within the first three hours after closed-head traumatic brain injury (TBI) and subarachnoid hemorrhage (SAH), two common traumatic vascular injuries, in mice. We took a multi-modal imaging approach using photoacoustic, color Doppler, and magnetic resonance imaging (MRI) in mice. Brain oxygenation (%sO2) and velocity-weighted volume of blood flow (VVF) values significantly decreased from baseline to fifteen minutes after both TBI and SAH. TBI resulted in 19.2% and 41.0% ipsilateral %sO2 and VVF reductions 15 minutes post injury while SAH resulted in 43.9% %sO2 and 85.0% VVF reduction ipsilaterally (p<0.001). We found partial recovery of %sO2 from 15 minutes to 3-hours after injury for TBI but not SAH. Hemorrhage, edema, reduced perfusion, and altered diffusivity were evident from MRI scans acquired 90-150 minutes after injury in both models although the spatial distribution was mostly focal for TBI and diffuse for SAH. The results reveal that the cerebral %sO2 deficits immediately following injuries are reversible for TBI and irreversible for SAH. Our findings can inform future studies on mitigating these early responses to improve long-term recovery., Comment: Update in order of figure panels for Figure 3

Published
2022

11. BK (Ca) nitrosylation is associated with cerebral microvascular dysfunction in female 5x-FAD mice

Author

Silva, Josiane F., Polk, Felipe D., Savu, Andrea, Kath, Allison M., Gee, Michael T., and Pires, Paulo W.

Subjects
Article
Abstract

Cerebral microvascular dysfunction and nitro-oxidative stress are present in patients with Alzheimer’s disease (AD) and may contribute to disease progression and severity. Large conductance Ca (2+) -activated K (+) channels (BK (Ca) ) play an essential role in vasodilatory responses and maintenance of myogenic tone in resistance arteries. BK (Ca) can be modified in a pro-nitro-oxidative environment, resulting in decreased activity and vascular hyper-contractility, which can compromise cerebral blood flow regulation. We hypothesized that reductions in BK (Ca) function in cerebral arteries, as a consequence of nitro-oxidative stress, are associated with blunted neurovascular responses in the 5x-FAD model of AD. Using pressure myography, we observed that posterior communicating arteries (PComA) from 5 months-old female 5x-FAD mice showed higher spontaneous myogenic tone than wild-type (WT) littermates. Constriction to the BK (Ca) blocker iberiotoxin (30 nM) was smaller in 5x-FAD than WT, suggesting lower basal BK (Ca) activity, which was independent of alterations in intracellular Ca (2+) transients or BK (Ca) mRNA expression. These vascular changes were associated with higher levels of oxidative stress in female 5x-FAD and a higher level of S-nitrosylation in the BK (Ca) α-subunit. In females, pre-incubation of PComA from 5x-FAD with the reducing agent DTT (10 µM) rescued iberiotoxin-induced contraction. Female 5x-FAD mice showed increased expression of iNOS mRNA, lower resting cortical perfusion atop the frontal cortex, and impaired neurovascular coupling responses. No significant differences between male 5x-FAD and WT were observed for all parameters above. These data suggest that the exacerbation in BK (Ca) S-nitrosylation contributes to cerebrovascular and neurovascular impairments in female 5x-FAD mice. SIGNIFICANCE STATEMENT: Cerebral vascular dysfunction is increasingly recognized as a hallmark of Alzheimer’s disease and other dementias. Impaired microvascular regulation can lead to deficits in blood flow to the brain. An intrinsic property of the resistance vasculature is to constrict when pressurized (myogenic tone), generating a vasodilatory reserve. Detrimental over-constriction is prevented by vascular feedback mechanisms, including the opening of large-conductance Ca (2+) -activated K (+) channels (BK (Ca) ). Here, using a combination of molecular biology tools with ex vivo and in vivo vascular assessments, we show a novel mechanism associated with BK (Ca) dysfunction in the cerebral microvasculature of female 5x-FAD mice. We report increased BK (Ca) S-nitrosylation linked to reduced activity and, consequently, higher basal myogenic tone. These changes were associated with lower perfusion of the frontal cortex and impaired neurovascular reactivity, suggesting that nitro-oxidative stress is an important mechanism of vascular dysfunction in Alzheimer’s disease.

Published
2023

18. Contributors

Author

Acharya, Tusar Kanta, Ahern, Gerard P., Al-Omari, Ammar, Ann, Jihyae, Aswin, Tanishaa, Banerjee, Anushka, Behrendt, Marc, Belvisi, Maria G., Bencze, Noémi, Bevan, Stuart, Bishnoi, Mahendra, Blumberg, Peter M., Bonvini, Sara J., Brain, Susan D., Campbell, James N., Cantero, María del Rocío, Cantiello, Horacio F., Chapman, Hugh, Charrua, A., Chung, Man-Kyo, Connolly, James, Cruz, F., Das, Nilesh Kumar, De Logu, Francesco, Dubey, Nishant Kumar, Erin, Nuray, Fallah, Hamideh P., Geppetti, Pierangelo, Goswami, Luna, Goswami, Chandan, Halder, Ramizur Rahaman, He, Qian, Helyes, Zsuzsanna, Holm, Patrik, Huang, Huizhen, Hudhud, Lina, Iannone, Luigi Francesco, Islas, Leon D., Jaffal, Sahar Majdi, Jalava, Niina, Kashio, Makiko, Kiselyov, Kirill, Koivisto, Ari, Konkoly, János, Kormos, Viktória, Kovács-Rozmer, Katalin, Kriszta, Gábor, Kuhad, Anurag, Kumar, Shamit, Kumar, Vikash, Kumar, Satish, Kumar, Abhishek, Lal, Roshan, Leavell, Yaowaree, Lee, Jeewoo, Liang, Dong, Liu, Yusheng, Lopez, Kyle E., Lyu, Yihan, Mahapatra, Parnasree, McKemy, David D., Mishra, Subham, Mohanta, Sushama, Nadezhdin, Kirill D., Nassini, Romina, Oláh, Attila, Patel, Mihir, Pepelyayeva, Yuliya, Pertovaara, Antti, Phan, Thieu X., Pintér, Erika, Pires, Paulo W., Pohóczky, Krisztina, Porszász, Robert, Pozsgai, Gábor, Puri, Priyanka, Rangel-Yescas, Gisela E., Rantanen, Marja, Rardin, Benjamin, Rokade, Tejas Pravin, Rosenberg, Paul, Ross, Sarah E., Royal, Mike A., Sahu, Ram Prasad, Savu, Andrea, Shikha, Deep, Silva, Josiane F., Simpson, David, Sing, Raima, Snyder, Lindsey M., Sobolevsky, Alexander I., Sodhi, Rupinder Kaur, Stevens, Randall, Szallasi, Arpad, Szőke, Éva, Szöllősi, Attila Gábor, Tóth, Attila, Tóth, Balázs István, Van Horn, Wade D., Wang, Hongmei, Wortley, Michael A., Zhang, Jinwei, and Zhou, Zirui

Published
2024
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20. sj-pdf-2-jcb-10.1177_0271678X211039592 - Supplemental material for Amyloid-β disrupts unitary calcium entry through endothelial NMDA receptors in mouse cerebral arteries

Author

Peters, Emily C, Gee, Michael T, Pawlowski, Lukas N, Kath, Allison M, Polk, Felipe D, Vance, Christopher J, Sacoman, Juliana L, and Pires, Paulo W

Subjects
110320 Radiology and Organ Imaging, FOS: Clinical medicine, FOS: Biological sciences, Medicine, Cell Biology, 110305 Emergency Medicine, 110306 Endocrinology, Biochemistry, 69999 Biological Sciences not elsewhere classified, 110904 Neurology and Neuromuscular Diseases, Neuroscience
Abstract

Supplemental material, sj-pdf-2-jcb-10.1177_0271678X211039592 for Amyloid-β disrupts unitary calcium entry through endothelial NMDA receptors in mouse cerebral arteries by Emily C Peters, Michael T Gee, Lukas N Pawlowski, Allison M Kath, Felipe D Polk, Christopher J Vance, Juliana L Sacoman and Paulo W Pires in Journal of Cerebral Blood Flow & Metabolism

Published
2021
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21. sj-pdf-1-jcb-10.1177_0271678X211039592 - Supplemental material for Amyloid-β disrupts unitary calcium entry through endothelial NMDA receptors in mouse cerebral arteries

Author

Peters, Emily C, Gee, Michael T, Pawlowski, Lukas N, Kath, Allison M, Polk, Felipe D, Vance, Christopher J, Sacoman, Juliana L, and Pires, Paulo W

Subjects
110320 Radiology and Organ Imaging, FOS: Clinical medicine, FOS: Biological sciences, Medicine, Cell Biology, 110305 Emergency Medicine, 110306 Endocrinology, Biochemistry, 69999 Biological Sciences not elsewhere classified, 110904 Neurology and Neuromuscular Diseases, Neuroscience
Abstract

Supplemental material, sj-pdf-1-jcb-10.1177_0271678X211039592 for Amyloid-β disrupts unitary calcium entry through endothelial NMDA receptors in mouse cerebral arteries by Emily C Peters, Michael T Gee, Lukas N Pawlowski, Allison M Kath, Felipe D Polk, Christopher J Vance, Juliana L Sacoman and Paulo W Pires in Journal of Cerebral Blood Flow & Metabolism

Published
2021
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25. Contributors

Author

Abou-Zamzam Jr., Ahmed M., Abularrage, Christopher J., AbuRahma, Ali F., AbuRahma, Zachary, Acher, Charles W., Acosta, Stefan, Adelman, Mark A., Akar, Ahmet Rüçhan, Aldailami, Hasan, Alimi Sr., Yves S., Arbabi, Cassra N., Arko III, Frank R., Armstrong, David G., Arnaoutakis, K. Dean J., Arora, Subodh, Arthurs, Zachary M., Ascher, Enrico, Avgerinos, Efthymios D., Azarbal, Amir F., Aziz, Faisal, Azizzadeh, Ali, Baba, Takeshi, Back, Martin, Baig, M. Shadman, Bailey, Charles J., Bailey, Christopher R., Ballast, Jocelyn K., Barnes, Geoffrey D., Bates, Mark C., Baumeister, Ruediger G.H., Beaulieu, Robert J., Bechara, Carlos F., Beck, Adam W., Belkin, Michael, Ben-Haim, Simona, Benjamin, Elizabeth R., Benjamin, Marshall E., Bernas, Michael J., Bismuth, Jean, Biteman, Benjamin R., Bivalacqua, Trinity J., Bjarnason, Haraldur, Björck, Martin, Black III, James H., Blankensteijn, Jan D., Blas, Joseph-Vincent V., Bose, Saideep, Bower, Thomas C., Bowling, Frank L., Brahmandam, Anand, Brewster, Luke, Brinster, Clayton J., Broce, Mike, Brody, Fredrick, Brooke, Benjamin S., Brown, Kellie R., Bush, Ruth L., Calligaro, Keith D., Campbell, John E., Carpenter, Jeffrey P., Carsten III, Christopher G., Cayne, Neal S., Chaer, Rabih A., Chang, Kevin Z., Chaturvedi, Shruti, Chauhan, Yusuf, Cheng, Charlie, Chinnadurai, Ponraj, Chou, Elizabeth, Clair, Daniel G., Clark, Ross M., Clouse, W. Darrin, Coleman, Dawn M., Colling, Meaghan E., Comerota, Anthony J., Conrad, Mark F., Conte, Michael S., Corriere, Matthew A., Dakour-Aridi, Hanaa, Dalman, Ronald L., Dalsing, Michael C., Dardik, Alan, Darling, R. Clement, III, Davies, Mark G., Davila, Victor J., Dawson, David L., Deery, Sarah E., Demetriades, Demetrios, P.M. de Vries, Jean-Paul, Diab, Kaled, Dillavou, Ellen D., DiMuzio, Paul, Dosluoglu, Hasan H., Dossabhoy, Shernaz S., Dougherty, Matthew J., Dryjski, Maciej L., Duncan, Audra A., Eagleton, Matthew J., Earnshaw, Jonothan J., Eberhardt, Robert T., Edwards, Jeffrey B., Edwards, Matthew S., Ehlert, Bryan A., Eidt, John F., Eldrup-Jorgensen, Jens, Eliason, Jonathan L., Elsayed, Nadin, Eskandari, Mark K., Eslami, Mohammad H., Farber, Alik, Farooqui, Emaad, Figueroa, C. Alberto, Fishman, Steven J., Flohr, Tanya R., Forbes, Thomas L., Fox, Charles, Freischlag, Julie A., Gandhi, Sagar S., Geary, Randolph L., Ghaffarian, Amir, Giuliano, Katherine, Glaudemans, Andor W.J.M., Gloviczki, Peter, Go, Michael R., Gober, Leah M., Goldman, Matthew P., Goodney, Philip P., Gowda, Mamatha, Grunebach, Holly, Guzman, Raul J., Hallett, John W., Hamdan, Allen D., Hansen, Kimberley J., Harris, Linda M., Hartung, Olivier, Haut, Elliott R., Hemingway, Jake F., Henke, Peter K., Hicks, Caitlin W., Hinchliffe, Robert J., Hingorani, Anil P., Ho, Karen J., Hohmann, Stephen E., Holscher, Courtenay M., Howell, Caronae, Hu, Yiyuan David, Humphries, Misty D., Hunter, Glenn C., Hurie, Justin, Iafrati, Mark D., Illig, Karl A., Inaba, Kenji, İnan, Mustafa Bahadır, Israel, Ora, Jacobowitz, Glenn R., Jaffer, Iqbal H., Jain, Krishna M., Jayaraj, Arjun, Johanning, Jason M., Johnson, Brad, Jordan Jr., William D., Kabbani, Loay S., Kabnick, Lowell S., Kalish, Jeffrey, Kalra, Manju, Kanthi, Yogendra, Kashyap, Vikram S., Kauffman, Paulo, Kauvar, David S., Kayssi, Ahmed, Kernodle, Amber B., Khan, Sikandar Z., Kiguchi, Misaki, Killeen, Amanda L., Kim, Gloria Y., Kim, Paul J., Kim, Tanner I., Kirkwood, Melissa L., Kleiss, Simone F., Knepper, Jordan, Kraiss, Larry W., Kwong, Jonathan M., Lajoie, Lidie, Lal, Brajesh K., Lala, Salim, LaMuraglia, Glenn M., Landry, Gregory J., Langford, John T., Laredo, James, Lawrence, Peter F., Lawson, Jeffrey H., Lavery, Lawrence A., Lee, Byung-Boong, Lee, Jason T., Lee, Young, Lely, Rutger J., Leong, Beatriz V., Levy, Elad l., Lewis, Anthony J., Li, Jing, Lillehei, Craig W., Lilly, Michael P., Lindsay, Thomas F., Lipsett, Pamela A., Lipsitz, Evan C., Litchfield, Terry F., Litt, Harold, Liu, James L., Liu, Zhao-Jun, Lohr, Joann M., Lugo, Joanelle, Lum, Ying Wei, Lurie, Fedor, Lynch, Thomas G., Ma, Kirsten F., Macsata, Robyn, Magee, Gregory A., Makaroun, Michel S., Malas, Mahmoud B., Maldonado, Thomas S., Malekpour, Fatemeh, Maleti, Oscar, Malka, Kimberly T., Mansour, M. Ashraf, Mansukhani, Neel A., Markovic, Jovan N., Marks, Natalie A., McCabe, Dominick J.H., McCarthy, Cullen K., McKinsey, James F., McLafferty, Robert B., McMurray, Robert C., McQuinn, Christopher W., Menard, Matthew T., Mendes, Bernardo C., Mills Sr., Joseph L., Milner, Ross, Modrall, J. Gregory, Mohebali, Jahan, Mokin, Maxim, Moneta, Gregory L., Money, Samuel R., Montross, Brittany C., Moore, Wesley S., Morasch, Mark, Morcos, Ramez, Mousa, Albeir Y., Muck, Patrick E., Myers, Daniel J., Myers, Stuart I., Nagarsheth, Khanjan H., Naoum, Joseph J., Naylor, A. Ross, Neville, Richard F., Nguyen, Bao-Ngoc, Nguyen, Louis L., Niklason, Laura E., Obi, Andrea, Ohki, Takao, Orion, Kristine C., Orlino, Jon P., Passman, Marc A., Patel, Rhusheet, Pearce, Benjamin J., Perler, Bruce A., Perry, Robert J.T., Pires, Paulo W., Plotkin, Anastasia, Powell, Richard J., Pruitt, Eric Yates, Puggioni, Alessandra, Quiñones-Baldrich, William J., Quiroga, Elina, Quiroz, Hallie, Raffetto, Joseph D., Raju, Seshadri, Recht, Matthew H., Reed, Amy B., Reilly, Brendon P., Reitz, Katherine M., Repella, Tana L., Rialon, Kristy L., Ricco, Jean-Baptiste, Rigberg, David A., Rios, Anthony L., Ritenour, Amber E., Robins, J. Eli, Rockman, Caron B., Rockson, Stanley G., Roddy, Sean P., Rogers, Lee C., Rohrer, Michael J., Rosenfeld, Ethan S., Ross, John R., Rossi, Peter J., Rowe, Vincent L., Roy, Rishi A., Russell, Todd E., Rzucidlo, Eva M., Sadek, Mikel, Salata, Konrad, Sam II, Albert D., Sarac, Timur P., Sarıcaoğlu, Mehmet Cahit, Satiani, Bhagwan, Schanzer, Andres, Schermerhorn, Marc L., Schlieder, Ian, Schneider, Joseph, Schneider, Peter A., Schwartz, Samuel, Scully, Rebecca E., Sen, Indrani, Shah, Samir K., Shames, Murray L., Shanmugam, Victoria K., Sharafuddin, Mel J., Sharma, Gaurav, Shepard, Alexander D., Shestopalov, Alexander, Shin, Laura, Shortell, Cynthia K., Sidawy, Anton N., Simons, Jessica P., Singh, Michael J., Singh, Niten, Siracuse, Jeffrey J., Slart, Riemer H.J.A., Smeds, Matthew R., Smith, Danielle C., Snow, Rachael, Soden, Peter A., Sorber, Rebecca A., Srivastava, Sunita D., Stanley, James C., Starnes, Benjamin W., Starr, Jean E., Stern, Jordan R., Sternbergh III, W. Charles, Stone, Patrick A., Stoner, Michael C., Sutzko, Danielle C., Tarpara, Anand, Taylor, Spence M., Thaveau, Fabien, Thompson, Jonathan R., Timaran, Carlos H., Tingen, Joseph S., Treffalls, John A., Troutman, Douglas A., Tsai, Lillian L., Tzeng, Edith, Ulloa, Jesus G., Upchurch Jr., Gilbert R., Valentine, R. James, Velazquez, Omaida C., Vo, Victoria, Vowels, Travis, Wakefield, Thomas W., Waqas, Muhammad, Wasan, Suman M., Wasse, Haimanot (Monnie), Weaver, Fred A., Weiss, Clifford R., Weitz, Jeffrey I., Westin, Gregory G., Williams, Carlin A., Williams, Timothy K., Williamson, Ashley J., Witte, Marlys H., Woelfel, Stephanie L., Wolosker, Nelson, Woo, Karen, Wynn, Martha, Yammine, Halim, Yan, Qi, Yeh, Chin-Chin C., Yoo, Taehwan, Yuo, Theodore H., Zarkowsky, Devin S., Zettervall, Sara L., and Zhou, Wei

Published
2023
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28. elife-35316-v2.pdf

Author

Pires, Paulo W. and Earley, Scott

Subjects
Physiology, FOS: Biological sciences, 111601 Cell Physiology, Biophysics, food and beverages, FOS: Basic medicine, 60603 Animal Physiology - Systems, psychological phenomena and processes
Abstract

Hypoxia and ischemia are linked to oxidative stress, which can activate the oxidant-sensitive transient receptor potential ankyrin 1 (TRPA1) channel in cerebral artery endothelial cells, leading to vasodilation. We hypothesized that TRPA1 channels in endothelial cells are activated by hypoxia-derived reactive oxygen species, leading to cerebral artery dilation and reduced ischemic damage. Using isolated cerebral arteries expressing a Ca2+ biosensor in endothelial cells, we show that 4-hydroxynonenal and hypoxia increased TRPA1 activity, detected as TRPA1 sparklets. TRPA1 activity during hypoxia was blocked by antioxidants and by TRPA1 antagonism. Hypoxia caused dilation of cerebral arteries, which was disrupted by antioxidants, TRPA1 blockade and by endothelial cell-specific Trpa1 deletion (Trpa1 ecKO mice). Loss of TRPA1 channels in endothelial cells increased cerebral infarcts, whereas TRPA1 activation with cinnamaldehyde reduced infarct in wildtype, but not Trpa1 ecKO, mice. These data suggest that endothelial TRPA1 channels are sensors of hypoxia leading to vasodilation, thereby reducing ischemic damage.

Published
2019
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29. The angiotensin II receptor type 1b is the primary sensor of intraluminal pressure in cerebral artery smooth muscle cells

Author

Pires, Paulo W, Ko, Eun-A, Pritchard, Harry A T, Rudokas, Michael, Yamasaki, Evan, and Earley, Scott

Subjects
Mice, Inbred C57BL, Mice, Knockout, Receptor, Angiotensin, Type 1/genetics, TRPM Cation Channels/physiology, Losartan/pharmacology, Angiotensin II Type 1 Receptor Blockers/pharmacology, cardiovascular system, Pressure, Animals, Cerebral Arteries/cytology, hormones, hormone substitutes, and hormone antagonists, circulatory and respiratory physiology, Myocytes, Smooth Muscle/physiology
Abstract

KEY POINTS: The angiotensin II receptor type 1b (AT1 Rb ) is the primary sensor of intraluminal pressure in cerebral arteries. Pressure or membrane-stretch induced stimulation of AT1 Rb activates the TRPM4 channel and results in inward transient cation currents that depolarize smooth muscle cells, leading to vasoconstriction. Activation of either AT1 Ra or AT1 Rb with angiotensin II stimulates TRPM4 currents in cerebral artery myocytes and vasoconstriction of cerebral arteries. The expression of AT1 Rb mRNA is ∼30-fold higher than AT1 Ra in whole cerebral arteries and ∼45-fold higher in isolated cerebral artery smooth muscle cells. Higher levels of expression are likely to account for the obligatory role of AT1 Rb for pressure-induced vasoconstriction. ABSTRACT: Myogenic vasoconstriction, which reflects the intrinsic ability of smooth muscle cells to contract in response to increases in intraluminal pressure, is critically important for the autoregulation of blood flow. In smooth muscle cells from cerebral arteries, increasing intraluminal pressure engages a signalling cascade that stimulates cation influx through transient receptor potential (TRP) melastatin 4 (TRPM4) channels to cause membrane depolarization and vasoconstriction. Substantial evidence indicates that the angiotensin II receptor type 1 (AT1 R) is inherently mechanosensitive and initiates this signalling pathway. Rodents express two types of AT1 R - AT1 Ra and AT1 Rb - and conflicting studies provide support for either isoform as the primary sensor of intraluminal pressure in peripheral arteries. We hypothesized that mechanical activation of AT1 Ra increases TRPM4 currents to induce myogenic constriction of cerebral arteries. However, we found that development of myogenic tone was greater in arteries from AT1 Ra knockout animals compared with controls. In patch-clamp experiments using native cerebral arterial myocytes, membrane stretch-induced cation currents were blocked by the TRPM4 inhibitor 9-phenanthrol in both groups. Further, the AT1 R blocker losartan (1 μm) diminished myogenic tone and blocked stretch-induced cation currents in cerebral arteries from both groups. Activation of AT1 R with angiotensin II (30 nm) also increased TRPM4 currents in smooth muscle cells and constricted cerebral arteries from both groups. Expression of AT1 Rb mRNA was ∼30-fold greater than AT1 Ra in cerebral arteries, and knockdown of AT1 Rb selectively diminished myogenic constriction. We conclude that AT1 Rb , acting upstream of TRPM4 channels, is the primary sensor of intraluminal pressure in cerebral artery smooth muscle cells.

Published
2017

43. Localized TRPA1 channel Ca 2+ signals stimulated by reactive oxygen species promote cerebral artery dilation

Author

Sullivan, Michelle N., primary, Gonzales, Albert L., additional, Pires, Paulo W., additional, Bruhl, Allison, additional, Leo, M. Dennis, additional, Li, Wencheng, additional, Oulidi, Agathe, additional, Boop, Frederick A., additional, Feng, Yumei, additional, Jaggar, Jonathan H., additional, Welsh, Donald G., additional, and Earley, Scott, additional

Published
2015
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48. Unitary TRPV3 channel Ca2+ influx events elicit endothelium-dependent dilation of cerebral parenchymal arterioles.

Author

Pires, Paulo W., Pritchard, Harry A. T., Earley, Scott, Sullivan, Michelle N., and Robinson, Jennifer J.

Subjects
*TRP channels, *CARVACROL, *COGNITION disorders, *HYPERPOLARIZATION (Cytology), *ENDOTHELIAL cells
Abstract

Cerebral parenchymal arterioles (PA) regulate blood flow between pial arteries on the surface of the brain and the deeper microcirculation. Regulation of PA contractility differs from that of pial arteries and is not completely understood. Here, we investigated the hypothesis that the Ca2+ permeable vanilloid transient receptor potential (TRPV) channel TRPV3 can mediate endothelium-dependent dilation of cerebral PA. Using total internal reflection fluorescence microscopy (TIRFM), we found that carvacrol, a monoterpenoid compound derived from oregano, increased the frequency of unitary Ca2+ influx events through TRPV3 channels (TRPV3 sparklets) in endothelial cells from pial arteries and PAs. Carvacrol-induced TRPV3 sparklets were inhibited by the selective TRPV3 blocker isopentenyl pyrophosphate (IPP). TRPV3 sparklets have a greater unitary amplitude (ΔF/F0 = 0.20) than previously characterized TRPV4 (AF/F0 = 0.06) or TRPA1 (AF/F0 = 0.13) sparklets, suggesting that TRPV3-mediated Ca2+ influx could have a robust influence on cerebrovascular tone. In pressure myography experiments, carvacrol caused dilation of cerebral PA that was blocked by IPP. Carvacrol-induced dilation was nearly abolished by removal of the endothelium and block of intermediate (IK) and small-conductance Ca2+-activated K+ (SK) channels. Together, these data suggest that TRPV3 sparklets cause dilation of cerebral parenchymal arterioles by activating IK and SK channels in the endothelium. [ABSTRACT FROM AUTHOR]

Published
2015
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