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Evangeline Motley-Johnson

TitleInterim Dean, School of Graduate Studies and Research
Faculty RankProfessor
InstitutionMeharry Medical College
DepartmentMicrobiology, Immunology, & Physiology
Address1005 Dr. D. B. Todd Blvd
Nashville TN 37208-3501
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    Collapse Biography 
    Collapse awards and honors
    2015Fellow, American Heart Association
    1989 - 1990Predoctoral Proter Development Fellowship, American Physiological Society
    1990Professional Opportunity Award, Proctor and Gamble
    1999Commitment and Perseverance in the Establishment of Research Award, Meharry Medical College
    1998Mentorship Award, Meharry Medical College, SOGSR
    2000Faculty Scholar Award, Meharry Medical College, SOGSR
    2001 - 2005Honored Member, America''s Registry of Outstanding Professionals
    2003Mentorship Award, Meharry Medical College, SOGSR
    2003Teaching Excellence Award, Meharry Medical College, SOGSR
    2004 - 2005Who''s Who Among America''s Teachers

    Collapse Overview 
    Collapse overview
    Evangeline D. Motley-Johnson, Ph.D. is a Professor and the Interim Chair of the Department of Physiology, and the Associate Dean of the School of Graduate Studies and Research. She received a B.A. in Biology from University of Virginia where she worked as a laboratory research assistant in the Department of Anesthesiology at the Medical Center studying the microvasculature of normotensive verse hypertensive animals. While working in this position, Dr. Motley decided to purse graduate studies at Howard University in Washington, D.C. where she received her Ph.D. in Physiology and Biophysics. Her dissertation research was completed in the Cardiovascular Research Division at SmithKline Beecham Pharmaceuticals in King of Prussia, PA where she studied the signal transduction pathways of alpha-1 and alpha-2 receptors in the vasculature. Dr. Motley pursued her postdoctoral studies in the Department of Pharmacology and Cell Biophysics at the University of Cincinnati in Ohio where she studied sodium-calcium exchange in the vasculature. She then joined the faculty in the Department of Physiology at Meharry Medical College as an Assistant Professor, and moved through the ranks to become a tenured Professor with her current administrative positions.

    Dr. Motley studies the cellular and molecular signal transduction pathways of G-protein-coupled receptors in the vascular wall of blood vessels, and how the dysfunction of these signaling pathways can contribute to cardiovascular diseases such as hypertension, atherosclerosis, and insulin resistance associated with diabetes. Dr. Motley’s lab has delineated the signaling pathway by which angiotensin II receptors cause cell proliferation, and currently, the lab is studying protease-activated receptor (PAR) signaling in endothelial cells. The lab has shown how PAR-1 and PAR-2 differentially activate endothelial nitric oxide synthase (eNOS) phosphorylation in the regulation of nitric oxide production, and current studies are delineating the role of other PARs, such as PAR-3 and PAR-4, in the signaling pathways that lead to vascular inflammation, cell migration, and proliferation in cardiovascular diseases. Understanding the signaling pathways involved in these diseases will allow therapeutic agents to be developed at the molecular level.

    Dr. Motley is well published in her field of research and is a member of several National Societies such as the American Physiological Society, the American Heart Association, and the Endocrine Society. She currently serves on National Committees and review panels. She has trained ten Ph.D. graduates and has taught physiology to graduate, medical and dental students. She also has trained many high school students and undergraduates as summer research fellows.

    The goal of my research is to delineate the signal transduction pathways that are involved in the development of cardiovascular diseases such as hypertension and atherosclerosis. I have studied various signaling pathways in my career starting with alpha-1 receptor signaling in the vasculature and then angiotensin II signaling. I am currently studying protease-activated receptor (PAR) signaling in endothelial cells and how it regulates endothelial nitric oxide synthase (eNOS) phosphorylation and nitric oxide (NO) production, which causes vasodilation in the vasculature. My lab has shown that PAR-1 and PAR-2 differentially activate eNOS by different signaling pathways. We have established that PAR-2 activation couples to Gq and a calcium-dependent signaling pathway to phosphorylate eNOS-Ser-1177, which leads to an increase in NO production, while PAR-1 activation couples to G12/13 and the Rho/ROCK signaling pathway to phosphorylate eNOS-Thr-495, which decreases NO production in human umbilical vein endothelial cells (HUVECs). In our current study, we hypothesize a differential coupling of PARs to the signaling pathways that regulate eNOS and NO production in primary adult human coronary artery endothelial cells (HCAECs). In this cell line, we observed that PAR-1 primarily couples to the signaling pathway that is responsible for the phosphorylation of eNOS-Ser-1177, and PAR-2 primarily couples to the the signaling pathway that is responsible for phosphorylation of eNOS-Thr-495. Our data suggests a vascular bed specific differential coupling of PARs to the signaling pathways that regulate eNOS and NO production that may be responsible for endothelial dysfunction associated with cardiovascular disease. In the future, we would like to further delineate the roles of PAR-3 and PAR-4 in the signaling pathways that lead to vascular inflammation, cell migration and proliferation in cardiovascular diseases.

    Collapse Research 
    Collapse research activities and funding
    T32HL007737     (VILLALTA, FERNANDO)Jul 1, 1993 - Jun 30, 2026
    Research Training in Cardiovascular Biology at Meharry
    Role: Co-Principal Investigator

    K14HL003320     (MOTLEY, EVANGELINE D)Sep 25, 1996 - Aug 31, 2001
    Role: Co-Principal Investigator

    R25GM059994     (MOTLEY-JOHNSON, EVANGELINE D)Aug 1, 1999 - Jul 31, 2022
    The Meharry RISE initiative
    Role: Principal Investigator

    SC3GM086336     (MOTLEY, EVANGELINE D)Feb 1, 2009 - Jan 31, 2012
    The Role of Protease-Activated Receptors in the Regulation of eNOS
    Role: Co-Principal Investigator

    Collapse Bibliographic 
    Collapse selected publications
    Publications listed below are automatically derived from MEDLINE/PubMed and other sources, which might result in incorrect or missing publications. Faculty can login to make corrections and additions.
    Newest   |   Oldest   |   Most Cited   |   Most Discussed   |   Timeline   |   Field Summary   |   Plain Text
    PMC Citations indicate the number of times the publication was cited by articles in PubMed Central, and the Altmetric score represents citations in news articles and social media. (Note that publications are often cited in additional ways that are not shown here.) Fields are based on how the National Library of Medicine (NLM) classifies the publication's journal and might not represent the specific topic of the publication. Translation tags are based on the publication type and the MeSH terms NLM assigns to the publication. Some publications (especially newer ones and publications not in PubMed) might not yet be assigned Field or Translation tags.) Click a Field or Translation tag to filter the publications.
    1. Tillery LC, Epperson TA, Eguchi S, Motley ED. Featured Article: Differential regulation of endothelial nitric oxide synthase phosphorylation by protease-activated receptors in adult human endothelial cells. Exp Biol Med (Maywood). 2016 Mar; 241(6):569-80. PMID: 26729042.
      Citations: 2     Fields:    Translation:HumansCells
    2. Miao L, Okoro EU, Cao Z, Yang H, Motley-Johnson E, Guo Z. High-density lipoprotein-mediated transcellular cholesterol transport in mouse aortic endothelial cells. Biochem Biophys Res Commun. 2015 Sep 18; 465(2):256-61. PMID: 26255968.
      Citations: 5     Fields:    Translation:AnimalsCells
    3. Watts VL, Motley ED. Role of protease-activated receptor-1 in endothelial nitric oxide synthase-Thr495 phosphorylation. Exp Biol Med (Maywood). 2009 Feb; 234(2):132-9. PMID: 19064940.
      Citations: 11     Fields:    Translation:HumansCells
    4. Motley ED, Eguchi K, Patterson MM, Palmer PD, Suzuki H, Eguchi S. Mechanism of endothelial nitric oxide synthase phosphorylation and activation by thrombin. Hypertension. 2007 Mar; 49(3):577-83. PMID: 17210830.
      Citations: 27     Fields:    Translation:HumansAnimalsCells
    5. Woolfolk EA, Eguchi S, Ohtsu H, Nakashima H, Ueno H, Gerthoffer WT, Motley ED. Angiotensin II-induced activation of p21-activated kinase 1 requires Ca2+ and protein kinase C{delta} in vascular smooth muscle cells. Am J Physiol Cell Physiol. 2005 Nov; 289(5):C1286-94. PMID: 16033904.
      Citations: 17     Fields:    Translation:AnimalsCells
    6. Shi M, Yang H, Motley ED, Guo Z. Overexpression of Cu/Zn-superoxide dismutase and/or catalase in mice inhibits aorta smooth muscle cell proliferation. Am J Hypertens. 2004 May; 17(5 Pt 1):450-6. PMID: 15110906.
      Citations: 16     Fields:    Translation:AnimalsCells
    7. Richardson SM, Maleque MA, Motley ED. 3-Morpholinosyndnonimine inhibits 5-hydroxytryptamine-induced phosphorylation of nitric oxide synthase in endothelial cells. Cell Mol Biol (Noisy-le-grand). 2003 Dec; 49(8):1385-9. PMID: 14984014.
      Citations: 1     Fields:    Translation:AnimalsCells
    8. Gardner CD, Eguchi S, Reynolds CM, Eguchi K, Frank GD, Motley ED. Hydrogen peroxide inhibits insulin signaling in vascular smooth muscle cells. Exp Biol Med (Maywood). 2003 Jul; 228(7):836-42. PMID: 12876303.
      Citations: 24     Fields:    Translation:AnimalsCells
    9. Motley ED, Eguchi K, Gardner C, Hicks AL, Reynolds CM, Frank GD, Mifune M, Ohba M, Eguchi S. Insulin-induced Akt activation is inhibited by angiotensin II in the vasculature through protein kinase C-alpha. Hypertension. 2003 Mar; 41(3 Pt 2):775-80. PMID: 12623995.
      Citations: 15     Fields:    Translation:AnimalsCells
    10. Motley ED, Kabir SM, Gardner CD, Eguchi K, Frank GD, Kuroki T, Ohba M, Yamakawa T, Eguchi S. Lysophosphatidylcholine inhibits insulin-induced Akt activation through protein kinase C-alpha in vascular smooth muscle cells. Hypertension. 2002 Feb; 39(2 Pt 2):508-12. PMID: 11882599.
      Citations: 22     Fields:    Translation:Animals
    11. Reynolds CM, Eguchi S, Frank GD, Motley ED. Signaling mechanisms of heparin-binding epidermal growth factor-like growth factor in vascular smooth muscle cells. Hypertension. 2002 Feb; 39(2 Pt 2):525-9. PMID: 11882602.
      Citations: 8     Fields:    Translation:AnimalsCells
    12. Motley ED, Kabir SM, Eguchi K, Hicks AL, Gardner CD, Reynolds CM, Frank GD, Eguchi S. Protein kinase C inhibits insulin-induced Akt activation in vascular smooth muscle cells. Cell Mol Biol (Noisy-le-grand). 2001 Sep; 47(6):1059-62. PMID: 11785657.
      Citations: 6     Fields:    Translation:AnimalsCells
    13. Frank GD, Eguchi S, Inagami T, Motley ED. N-acetylcysteine inhibits angiotensin ii-mediated activation of extracellular signal-regulated kinase and epidermal growth factor receptor. Biochem Biophys Res Commun. 2001 Feb 02; 280(4):1116-9. PMID: 11162642.
      Citations: 9     Fields:    Translation:AnimalsCells
    14. Frank GD, Eguchi S, Yamakawa T, Tanaka S, Inagami T, Motley ED. Involvement of reactive oxygen species in the activation of tyrosine kinase and extracellular signal-regulated kinase by angiotensin II. Endocrinology. 2000 Sep; 141(9):3120-6. PMID: 10965882.
      Citations: 22     Fields:    Translation:AnimalsCells
    15. Numaguchi K, Eguchi S, Yamakawa T, Motley ED, Inagami T. Mechanotransduction of rat aortic vascular smooth muscle cells requires RhoA and intact actin filaments. Circ Res. 1999 Jul 09; 85(1):5-11. PMID: 10400905.
      Citations: 45     Fields:    Translation:AnimalsCells
    16. Mathias SA, Mgbonyebi OP, Motley E, Owens JR, Mrotek JJ. Modulation of adrenal cell functions by cadmium salts. 4. Ca(2+)-dependent sites affected by CdCl2 during basal and ACTH-stimulated steroid synthesis. Cell Biol Toxicol. 1998 Jun; 14(3):225-36. PMID: 9689495.
      Citations:    Fields:    Translation:AnimalsCells
    17. Onaivi ES, Bishop-Robinson C, Motley ED, Chakrabarti A, Chirwa SS. Neurobiological actions of cocaine in the hippocampus. Ann N Y Acad Sci. 1996 Oct 31; 801:76-94. PMID: 8959025.
      Citations: 4     Fields:    Translation:Animals
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