David A. Tulis, MS, Ph.D., F.A.H.A.

Portrait of David Tulis

Associate Professor

Master Educator, Office of Faculty Affairs & Leadership Development, Brody School of Medicine, East Carolina University

Director, Summer Scholars Research Program (SSRP), Office of Medical Education, Brody School of Medicine, East Carolina University

Director, Research Distinction Track, Office of Medical Education, Brody School of Medicine, East Carolina University

Phone: 252-744-2771
E-mail: tulisd@ecu.edu

Research Interests

Cardiovascular disease (CVD) ranks as the number one killer of Americans and individuals worldwide, yet unfortunately many of the mechanisms that contribute to CVD remain unclear. The primary focus of research in Dr. Tulis’ laboratory is identification and characterization of some of the biochemical, molecular, cellular, and functional mechanisms that underlie abnormal blood vessel growth, a major element of CVD. Our hope is that through these efforts we will be able to identify novel players in the development and/or maintenance of CVD which could then serve as potential therapeutic targets to combat these dreaded diseases.

There are several ongoing areas of study in our laboratory that focus on cardiac and vascular physiology and pathology, and these include acid-/pH-sensing receptors and ion channels, unique aspects of transcriptional/translational control, and cyclic nucleotide/protein kinase signaling. Some of our more exciting work recently has focused on ischemic hypoxia and novel avenues for control. Biochemical, molecular, cellular, and functional approaches are used including gain-of-function/loss-of-function interventions (viral/plasmid/RNAi/etc.) and in vivo, ex vivo and in vitro models. We hope that results from our studies will shed light on potentially promising strategies that could minimize the severity of CVD and associated vascular growth disorders and that may offer beneficial prospects for further study in basic science and clinical studies.

Education & Training

  • Post-doctoral Fellow, Division of Hematology and Oncology, Department of Medicine, Baylor College of Medicine, Houston, TX
  • Post-doctoral Fellow, Department of Biomedical Engineering, Rice University, Houston, TX
  • Doctor of Philosophy, Biomedical Sciences (Cardiovascular Sciences Tract), Eastern Virginia Medical School & Old Dominion University, Norfolk, VA
  • Master of Science, Toxicology (major), Genetics (minor), North Carolina State University, Raleigh
  • Bachelor of Science, Biology, University of North Carolina at Chapel Hill

Selected Publications

  • Tulis, D.A., Fishbein, I. Editorial: Animal Models of Vascular Interventions. Front. Cardiovasc. Med.; 2025.
  • Williams, M.D., Morgan, J.S., Bullock, M.T., Poovey, C.E., Wisniewski, M.E., Francisco, J.T., Barajas-Nunez, J.A., Hijazi, A.M., Theobald, D., Sriramula, S. Mansfield, K.D., Holland, N.A., Tulis, D.A.  pH-sensing GPR68 inhibits vascular smooth muscle cell proliferation through Rap1A. Am. J. Physiol. Heart Circ. Physiol. 327:H1210-1229; doi:10.1152/ajpheart.00413.2024; 2024.
  • Williams, M.D., Bullock, M.T., Johnson, S.C., Holland, N.A., Vuncannon, D.M., Zary Oswald, J., Adderley, S.P., Tulis, D.A.Protease-activated receptor 2 controls vascular smooth muscle cell proliferation in cyclic AMP-dependent protein kinase/mitogen-activated protein kinase kinase 1/2-dependent manner. J. Vasc. Res. 60:213-226; doi:10.1159/000532032; 2023.
  • Tulis, D.A., McNeish, A.J. Editorial: Rising Stars in Vascular Physiology. Front. Physiol. 14:1278632; doi:10.3389/fphys.2023.1278632; 2023.
  • Francisco, J.T., Holt, A.W., Bullock, M.T., Williams, M.D., Poovey, C.E., Holland, N.A., Brault, J.J., Tulis, D.A.FoxO3 normalizes Smad3-induced arterial smooth muscle cell growth. Front. Physiol. 14.1136998; doi: 10.3389/fphys.2023.1136998; 2023.
  • Strom, C.J., McDonald, S.M., Kew, K.A., Houmard, J.A., Tulis, D.A., Pawlak, R., Kelley, G.A., Chasen-Taber, L., Newton, E., Isler, C., DeVente, J., Wisseman, B., May, L.E.A narrative review of the individual benefits of maternal exercise or PUFA supplementation during pregnancy: Are we missing something?Acta Scientific Women’s Health 4.9: 12-22; 2022.
  • Strom, C.J., McDonald, S.M., Remchak, M-M., Kew, K.A., Rushing, B.R., Houmard, J.A., Tulis, D.A., Pawlak, R., Kelley, G.A., Chasen-Taber, L., Newton, E., Isler, C., DeVente, J., Raper, M., May, L.E.Maternal aerobic exercise, but not blood docasahexaenoic acid and eicosapentaenoic acid concentrations, during pregnancy influence infant body composition. Int. J. Environ. Res. Public Health 19(14): 8293; 2022.
  • Strom, C.J., McDonald, S.M., Remchak, M-M., Kew, K.A., Rushing, B.R., Houmard, J.A., Tulis, D.A., Pawlak, R., Kelley, G.A., Chasen-Taber, L., Newton, E., Isler, C., DeVente, J., Raper, M., May, L.E.The influence of maternal aerobic exercise, blood DHA and EPA concentrations on maternal lipid profiles.Int. J. Environ. Res. Public Health 19(6), 3550; 2022.
  • Davis, P.R., Miller, S.G., Verhoeven, N.A., Morgan, J.S., Tulis, D.A., Witczak, C.A., Brault, J.J. Increased AMP deaminase activity decreases ATP content and slows protein degradation in cultured skeletal muscle.Metabolism 2020 May 1; 154257; doi:10.1016/j.metabol.2020.154257; 2020.
  • Holland, N., Francisco, J., Johnson, S., Morgan, J., Dennis, T., Gadireddy, N., Tulis, D.  Cyclic nucleotide-directed protein kinases in cardiovascular inflammation and growth.J. Cardiovasc. Dev. Dis. 5(1), 6; doi:10.3390/jcdd5010006, 2018.
  • Tulis, D.A.  Novel protein kinase targets in vascular smooth muscle therapeutics.  Curr. Opin. Pharmacol. 33: 12-16, 2017.
  • Holt, A.W., Howard, W.E., Ables, E.T., George, S.M., Kukoly, C.A., Rabidou, J.E., Francisco, J.T., Chukwu, A.N., Tulis, D.A.  Making the cut: Innovative methods for optimizing perfusion-based migration assays.  Cytometry Part A 91:270-280; 2017.
  • Stone, J.D., Holt, A.W., Shaver, P.R., Vuncannon, J.R., Tulis, D.A.  AMP-activated protein kinase inhibits arterial smooth muscle cell proliferation in vasodilator-stimulated phosphoprotein-dependent manner.  J. Non-Inv. Vasc. Invest. 1:002, 2016.
  • Holt, A.W., Martin, D.N., Shaver, P.R., Adderley, S.P., Stone, J.D., Joshi, C.N., Francisco, J.T., Lust, R.M., Weidner, D.A., Shewchuk, B.M., Tulis, D.A.  Soluble guanylyl cyclase-activated cyclic GMP-dependent protein kinase inhibits arterial smooth muscle cell migration independent of VASP-Serine 239 phosphorylation.  Cell. Signal. 28: 1364-1379, doi:10.1016/j.cellsig.2016.06.012, 2016.
  • Stone, J.D., Holt, A.W., Vuncannon, J.R., Brault, J.J., Tulis, D.A.  AMP-activated protein kinase inhibits transforming growth factor-β-mediated vascular smooth muscle cell growth: Implications for a Smad-3-dependent mechanism. Am. J. Physiol. Heart Circ. Physiol. 309: H1251-H1259; doi:10.1152/ajpheart.00846.2014, 2015.
  • Adderley, S.P., Martin, D.N., Tulis, D.A.  Exchange protein activated by cAMP (EPAC) controls migration of vascular smooth muscle cells in concentration- and time-dependent manner.  Arch. Physiol. 2:2, doi: http://dx.doi.org/10.7243/2055-0898-2-2, 2015.
  • Joshi, C.N., Tulis, D.A.  Connexins and intercellular communication in arterial growth and remodeling.  Arch. Physiol. 2:1; http://dx.doi.org/10.7243/2055-0898-2-1, 2015.
  • Johnson, T.L., Tulis, D.A.*, Keeler, B.E., Virag, J.A., Lust, R.M., Clemens, S.C.  The dopamine D3 receptor knockout mouse mimics aging-related changes in autonomic function and cardiac fibrosis.  PLoS ONE 8(8): e74116. doi:10.1371/ journal.pone.0074116, 2013. [* co-first author]
  • Holt, A.W., Tulis, D.A.  Experimental rat and mouse carotid artery surgery: Injury & remodeling studies. ISRN Minimally Invasive Surgery, Article No. 167407, http://dx.doi.org/ 10.1155/2013/167407, 2013.
  • Stone, J.D., Narine, A., Shaver, P.R., Fox, J.C., Vuncannon, J.R., Tulis, D.A.  AMP-activated protein kinase inhibits vascular smooth muscle cell proliferation and migration and vascular remodeling following injury.  Am. J. Physiol. Heart Circ. Physiol. 304: H369-H381, 2013.
  • Stone, J.D., Narine, A., Tulis, D.A.  Inhibition of vascular smooth muscle growth via signaling crosstalk between AMP-activated protein kinase and cAMP-dependent protein kinase.  Front. Physiol. 3:409.  doi: 10.3389/fphys.2012.00409, 2012.
  • Joshi, C.N., Martin, D.N., Shaver, P., Madamanchi, C., Muller-Borer, B.J., Tulis, D.A.  Control of vascular smooth muscle cell growth by connexin 43.  Front. Physiol.  3:220; doi: 10.3389/fphys.2012.00220, 2012.
  • Peyton, K.J., Shebib, A.R., Azam, M.A., Liu, X., Tulis, D.A., Durante, W.  Bilirubin inhibits neointima formation and vascular smooth muscle cell proliferation and migration.  Front. Pharmacol. 3:48; doi: 10.3389/fphar.2012.00048, 2012.
  • Adderley, S.P., Joshi, C.N., Martin, D.N., Tulis, D.A.  Phosphodiesterases regulate BAY 41-2272-induced VASP phosphorylation in vascular smooth muscle cells. Front. Pharmacol. 3:10; doi:10.3389/fphar.2012.00010, 2012.
  • Joshi, C.N., Martin, D.N., Fox, C.J., Mendelev, N.N., Brown, T.A., Tulis, D.A.  The soluble guanylate cyclase stimulator BAY 41-2272 inhibits vascular smooth muscle growth through the protein kinase A and protein kinase G pathways.  J. Pharmacol. Exp. Ther. 339: 394-402, 2011.
  • Keswani, A.N., Peyton, K.J., Durante, W., Schafer, A.I., and Tulis, D.A.The cyclic GMP modulators YC-1 and zaprinast reduce vessel remodeling through anti-proliferative and pro-apoptotic effects.J. Cardiovasc. Pharm. Ther. 14 (2): 116-124, 2009.
  • Peyton, K.J., Ensenat, D., Azam, M.A., Keswani, A.N., Sankaranaryanan, K., Liu, X.M., Wang, H., Tulis, D.A., and Durante, W.Arginase promotes neointima formation in rat injured carotid arteries.Arterioscler. Thromb. Vasc. Biol. 29 (4): 488-494, 2009.
  • Mendelev, N.N., Williams, V.S., and Tulis, D.A.Anti-growth properties of BAY 41-2272 in vascular smooth muscle cells.J. Cardiovasc. Pharmacol. 53 (2): 121-131, 2009.
  • Liu, X.M., Peyton, K.J., Mendelev, N.N., Wang, H., Tulis, D.A., and Durante, W.YC-1 stimulates the expression of gaseous monoxide-generating enzymes in vascular smooth muscle cells.Mol. Pharmacol. 75: 1-10, 2009.
  • Tulis, D.A.  Novel therapies for cyclic GMP control of vascular smooth muscle growth.  American J. Therapeutics 15: 551-564, 2008.
  • Mukhopadhyay, S. and Tulis, D.A.  Endocannabinoid regulation of matrix metalloproteinases: implications in ischemic stroke.Cardiovasc. Hematol. Agents Med. Chem. 5 (4), 311-318, 2007.
  • Tulis, D.A.  Rat carotid artery balloon injury model. Methods Mol. Med., 139: 1-30, 2007.
  • Tulis, D.A. Histological and morphometric analyses for rat carotid artery balloon injury studies. Methods Mol. Med. 139: 31-66, 2007.
  • Jackson, E., Mukhopadhyay, S., and Tulis, D.A.  Pharmacologic modulators of soluble guanylate cyclase/cyclic guanosine monophosphate in the vascular system – from benchtop to bedside.Curr. Vasc. Pharmacol. 5 (1): 1-14, 2007.
  • Tulis, D.A.  Methods for identifying cardiovascular agents: A review.  Recent Pat. Cardiovasc. Drug Disc. 1: 47-56, 2006.
  • Yang, X., Thomas, D.P., Zhang, X., Culver, B., Alexander, B.M., Murdoch, W.J., Tulis, D.A., Ren, J., and Sreejayan, N.Curcumin inhibits PDGF-stimulated vascular smooth muscle cell function and injury-induced neointima formation.Arterioscler. Thromb. Vasc. Biol. 26: 85-90, 2006.
  • Tulis, D.A., Keswani, A.N., Peyton, K.J., Wang, H., Schafer, A.I., Durante, W.  Local administration of carbon monoxide inhibits neointima formation in balloon injured rat carotid arteries.  Cell. Mol. Biol. (Noisy-le-grand) 51:441-446, 2005.
  • Bohl Masters, K.S., Lipke, E.A., Rice, E.E.H., Liel, M.S., Myler, H.A., Zygourakis, C., Tulis, D.A., and West, J.L.Nitric oxide-generating hydrogels inhibit neointima formation.J. Biomater. Sci. Polym. Ed. 16: 659-672, 2005.
  • Tulis D.A.Salutary properties of YC-1 in the cardiovascular and hematological systems.  Curr. Med. Chem. Cardiovasc. Hematol. Agents 2: 343-359, 2004.
  • Tulis, D.A., Mnjoyan, Z.H., Schiesser, R.L., Shelat, H.S., Evans, A.J., Zoldhelyi, P., and Fujise, K.  Adenoviral gene transfer of fortilin attenuates neointima formation through suppression of vascular smooth muscle cell proliferation and migration.  Circulation 107: 98-105, 2003.
  • Yuan, Y., Liao, L., Tulis, D.A., and Xu, J.Steroid receptor coactivator-3 is required for inhibition of neointima formation by estrogen.Circulation 105: 2653-2659, 2002.
  • Tulis, D.A., Bohl Masters, K.S., Lipke, E.A., Schiesser, R.L., Evans, A.J., Peyton, K.J., Durante, W., West, J.L., and Schafer, A.I.  YC-1-mediated vascular protection through inhibition of smooth muscle cell proliferation and platelet function. Biochem. Biophys. Res. Commun. 291: 1014-1021, 2002.
  • Tulis, D.A., Durante, W., Liu, X.M., Evans, A.J., Peyton, K.J., and Schafer, A.I.  Adenovirus-mediated heme oxygenase-1 gene delivery inhibits injury-induced vascular neointima formation.  Circulation 104: 2710-2715, 2001.
  • Tulis, D.A., Durante, W., Peyton, K.J., Evans, A.J., and Schafer, A.I.  Heme oxygenase-1 attenuates vascular remodeling following balloon injury in rat carotid arteries.  Atherosclerosis 155: 113-122, 2001.
  • Tulis, D.A., Durante, W., Peyton, K.J., Chapman, G.B., Evans, A.J., and Schafer, A.I.  YC-1, a benzyl indazole derivative, stimulates vascular cGMP and inhibits neointima formation.  Biochem. Biophys. Res. Comm. 279: 646-652, 2000.
  • Tulis, D.A., and Prewitt, R.L.  Medial and endothelial platelet-derived growth factor A chain expression is regulated by in vivo exposure to elevated flow.  J. Vasc. Res. 35: 413-420, 1998.
  • Tulis, D.A., Unthank, J.L., and Prewitt, R.L. Flow-induced arterial remodeling in rat mesenteric vasculature.  Am. J. Physiol. 274 (Heart Circ. Physiol. 43): H874-H882, 1998.

Selected Peer-reviewed Book Chapters

  • Tulis, D.A., Middlemas, D.S.  Vasodilators for Hypertensive Crises, Pulmonary Hypertension, and Erectile Dysfunction.  Brody’s Human Pharmacology: Mechanism-Based Therapeutics, Seventh Edition, Chapter 41, pp. 359-366, Eds. L. Wecker & S.L. Ingram; Elsevier Publishing; ISBN 978-0-323-84673-8; 2025.
  • Tulis, D.A., Middlemas, D.S.  Vasodilators for Hypertensive Crises, Pulmonary Hypertension, and Erectile Dysfunction. Brody’s Human Pharmacology: Mechanism-Based Therapeutics, Sixth Edition, Chapter 41, pp. 330-336, Eds. L. Wecker, D.A. Taylor, R.J. Theobald, Jr.; Elsevier Publishing; ISBN 978-0-323-47652-2; 2019.
  • Holland, N., Francisco, J., Johnson, S., Morgan, J., Dennis, T., Gadireddy, N., Tulis, D.  Cyclic nucleotide-directed protein kinases in cardiovascular inflammation and growth. In: Cyclic Nucleotide Signaling and the Cardiovascular System, Chapter 17, pp. 229-258; Ed. T. Brand, E. Klussmann, MDPI Books; 2018.
  • Holt, D., de Castro Brás, L., Tulis, D.  Cyclic Nucleotide-driven Protein Kinase Signaling in Arterial Smooth Muscle (Patho)physiology, Coronary Artery Disease – Causes, Symptoms & Treatments, 1st Edition, iCONCEPT Press, Ltd., ISBN:978-1-922227-92-8. iConcept Press, 2016.
  • Holt, D., Tulis, D.  Vascular Smooth Muscle as a Therapeutic Target in Disease Pathology. Muscle Cell and Tissue, Chapter 1, pp. 3-26, Ed. K. Sakuma, InTech Open Access Publishers, ISBN 978-953-51-2156-5, doi: 10.5772/60878; http://www.intechopen.com/articles/show/title/vascular-smooth-muscle-as-a-therapeutic-target-in-disease-pathology, 2015.
  • Tulis, D.A.  Novel Cyclic Nucleotide Signals in the Control of Pathologic Vascular Smooth Muscle Growth, Cardiovascular Disease II, 1st Edition, Chapter 9, pp. 175-200, iCONCEPT Press, Ltd., ISBN 978-1-922227-560, https://www.iconceptpress.com/books/042-2-1/cardiovascular-disease-ii/, 2014.
  • Adderley, S.P., Joshi, C.N., Martin, D.N., Mooney, S., Tulis, D.A.  Multiple Kinase Involvement in the Regulation of Vascular Growth, Advances in Protein Kinases, Chapter 6, pp. 131-150, Ed. G. Da Silva Xavier, InTech Open Access Publishers, ISBN 978-953-51-0633-3, 2012.

Selected Grants

  • A central-peripheral B1R/GPR68 axis in hypertension (Tulis, PI); ECU Sponsored Activities and Research Catalyst Program (SPARC); Office of Research Development, Research, Economic Development & Engagement
  • Regulation of the vascular growth response to ischemia/hypoxia by acid-sensing GPR68 (Tulis, PI); Brody Brothers Endowment Fund, ECU Medical & Health Sciences Foundation
  • Ischemic vascular disease: determining plasma membrane acid/base status in a ‘SNAP’ (Tulis, PI); Biomaterials Research Cluster, ECU Department of Engineering
  • Acid-sensing GPCRs in vascular inflammation and growth (Tulis, PI); NIH/NHLBI R15 HL135669
  • Cyclic GMP/Smad3/FoxO3 control of vascular smooth muscle growth (Tulis, PI); ECU Intramural Research Award, Division of Research, Economic Development and Engagement
  • Acidosis signaling pathways in diabetic vasculopathy (Tulis, PI); Brody Brothers Endowment Fund, East Carolina University Medical & Health Sciences Foundation
  • Function and signaling of GPR4 in vascular response to ischemia-related acidosis (Yang, PI; Tulis, Co-I); American Heart Association, National Affiliate, Scientist Development Grant
  • The proton-sensing G protein-coupled receptors GPR4 and GPR68 in abnormal vascular growth (Tulis, PI; Yang, Co-I); Brody School of Medicine, ECU
  • Role of GPR4 receptor in blood vessels (Yang, PI; Tulis, Co-I); Brody School of Medicine, ECU
  • Acidosis signaling pathways in vascular complications of diabetes (Tulis, PI; Yang, Co-I); declined; Interdisciplinary Research Award, Division of Research and Graduate Studies, ECU
  • Acidosis, hypoxia, and glucose deprivation pathways in endothelial inflammation (Yang, PI; Tulis Co-I); declined; Interdisciplinary Research Award, Division of Research and Graduate Studies, ECU
  • AMP kinase control of vascular growth (Stone, PI; Tulis, Mentor); American Heart Association, Mid-Atlantic Affiliate, Pre-doctoral Fellowship
  • NO-independent cGMP regulation of vascular remodeling (Tulis, PI); Research Supplement to Promote Diversity in Health-Related Research; NIH/NHLBI R01 HL081720-05S1
  • NO-independent cGMP regulation of vascular remodeling (Tulis, PI); American Recovery and Reinvestment Act (ARRA) Funds for Administrative Supplement; NIH/NHLBI R01 HL081720-03S2
  • NO-independent cGMP regulation of vascular remodeling (Tulis, PI); American Recovery and Reinvestment Act (ARRA) Funds for Administrative Supplement for Students and Science Educators; NIH/NHLBI R01 HL081720-03S1
  • NO-independent cGMP regulation of vascular remodeling (Tulis, PI); NIH/NHLBI R01 HL081720
  • A salutary role for soluble guanylate cyclase and cyclic guanosine monophosphate in regulating the arterial response to injury (Tulis, PI);
  • The role of carbon monoxide as a physiologic regulator of the arterial remodeling response to endovascular injury (Tulis, PI); American Heart Association, Beginning Grant-In-Aid, Texas Affiliate, Baylor College of Medicine, Houston, TX
  • The role of carbon monoxide as a physiologic regulator of the arterial remodeling response to endovascular injury (Tulis, PI);
  • The role of carbon monoxide as a physiologic regulator of the arterial remodeling response to endovascular injury (Tulis, PI);
  • The role of carbon monoxide as a physiologic regulator of the arterial remodeling response to endovascular injury (Tulis, PI); The Methodist Hospital Foundation Grant; Baylor College of Medicine, Houston, TX

Selected Editorial & Advisory Service

  • American Heart Association, Career Development Award; Vascular Endothelial Biology & Function Study Section
  • NIH, Respiratory, Cardiac and Circulatory System (RCCS) Branch; Special Emphasis Panel Study Section; ZRG1-RCCS-B
  • Eastern Area Health Education Center (AHEC); Scholars Regional Advisory Committee
  • Review Editor, Editorial Board; Frontiers in Endocrinology
  • Associate Editor, Associate Editorial Board; Frontiers in Cardiovascular Medicine
  • International Consortium for Personalized Medicine (IC PerMed), The Italian Ministry of Health; Study Section
  • American Heart Association, Innovative Project Award; Basic Sciences 1; Study Section
  • American Heart Association, Vascular Biology & Blood Pressure Fellowship Grant; Study Section
  • Review Editor, Redox Physiology; Editorial Board; Frontiers in Physiology
  • Associate Editor, Associate Editorial Board; Frontiers in Physiology
  • Associate Editor, Cardiovascular and Smooth Muscle Pharmacology; Associate Editorial Board, Frontiers in Pharmacology
  • American Heart Association, Vascular Biology & Blood Pressure Fellowship Grant; Study Section
  • United Kingdom Research & Innovation (UKRI), Medical Research Council; Study Section
  • American Heart Association, Vascular Biology & Blood Pressure Basic Science; Fellowship Grant Study Section
  • The French National Program of Clinical Research (PHRC), Ministry of Health France; Study Section
  • American Heart Association, Career Development Award Vascular Basic Sciences; Study Section
  • American Heart Association, Mentoring for Professionals
  • American Heart Association, Vascular Biology and Blood Pressure BSc; Study Section
  • NIH RCMI U54 Consortium Grant; Study Section
  • Italian Medicines Agency (AIFA), The Italian Ministry of Health; Study Section
  • The French National Research Agency (ANR); Study Section
  • French Intensive Care Society, Society of Resuscitation of French Language (FICS-SRLF); Study Section
  • Editorial Board, Journal of Non-Invasive Vascular Investigation; Italian Society for Vascular Investigation
  • Medical Research Council, United Kingdom Shared Business Services Ltd.; Study Section
  • Senior Editor, Archives of Physiology
  • French Intensive Care Society, Society of Resuscitation of French Language (FICS-SRLF); Study Section
  • American Heart Association, National, Innovative Research Grant; Vascular Science 1; Study Section, Chair
  • Editorial Board, Archives of Physiology
  • Review Editor, Frontiers in Physiology
  • Editorial Board, Frontiers in Pharmacology
  • Editorial Board, Frontiers in Vascular Physiology; Frontiers in Physiology
  • American Physiological Society; Cardiovascular Section Advocacy Committee
  • The Wellcome Trust & Royal Society; London, United Kingdom; Study Section
  • American Heart Association, National, Innovative Research Grant; Vascular Science 1; Study Section, Co-Chair
  • American Heart Association, National, Innovative Research Grant; Vascular Regulation & Disease; Study Section
  • Editorial Board, Frontiers in Genomic Physiology; Frontiers in Physiology
  • Editorial Board, Frontiers in Integrative and Regenerative Pharmacology; Frontiers in Pharmacology
  • Sigma Delta Epsilon, Graduate Women in Science; National Fellowships Committee; Study Section
  • Center for Scientific Review, National Institutes of Health & The Italian Ministry of Health, Directorate for Health and Technologies Research; Study Section
  • American Heart Association, Region II Vascular Wall Biology; Study Section
  • Editorial Board, Recent Patents on Cardiovascular Drug Discovery; Bentham Science Publishers, Ltd.
  • American Heart Association, Mid-Atlantic Affiliate; Vascular Wall Biology, Thrombosis, Microprote