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Jonathan H. Jaggar, Ph.D.

April 1, 2014

Department of Physiology
University of Tennessee Health Science Center
Memphis, TN


From left to right: Jonathan Jaggar, Xue (Roger) Zhai, Andrelina Noronha, Sarah Burris, Michael Kidd, Brent Williams, Dennis Leo, Qian Wang, Kirk Evanson, Simon Bulley. Not pictured - John Bannister

Primary Research:

My research program studies physiological functions and pathological alterations in ion channels in arterial smooth muscle cells. A major focus is to understand mechanisms by which ion channels control arterial contractility. Our work has identified novel signaling mechanisms and physiological functions of arterial smooth muscle local and global calcium signals, mitochondria, IP3 receptors, Cav1.2 channels, TRP channels, Ca2+-activated Cl- channels, BKCa channels and carbon monoxide and hydrogen sulfide, endogenous physiological gas transmitters. Recently, we have become particularly interested in investigating the functional significance and mechanisms involved in ion channel trafficking in arterial smooth muscle cells. Research in my laboratory uses a wide variety of molecular, biochemical, cellular, and functional techniques and cardiovascular disease and transgenic animal models.

Find more information on the web:

Lab Members:

John Bannister, Ph.D. University of Leeds, United Kingdom

Postdoctoral Fellows
Sarah Burris, Ph.D. St. Louis University
Simon Bulley, Ph.D. Florida Atlantic University
Qian Wang, Ph.D. University of Queensland, Australia
Kirk Evanson, Ph.D. University of Arkansas
Dennis Leo, Ph.D. Indian Veterinary Research Institute

Graduate Students
Michael Kidd, B.S. UC, San Diego
Xue (Roger) Zhai, B.S. Nankai University, China

Visiting Scientist
Andrelina Noronha, Ph.D. University of Ceará, Brazil

Technical Staff
Brent Williams, B.S., Ph.D., Tulane University

Number of trainees in the laboratory: 10

Recent Publications:

Bannister, JP, Adebiyi, A, Zhao, G, Narayanan, D, Thomas, CM, Feng, JY, & Jaggar, JH. (2009). Smooth muscle cell α2δ-1 subunits are essential for vasoregulation by CaV1.2 channels. Circulation Research, 105, 948-955. PMID: 19797702

Adebiyi, A, Zhao, G, Narayanan, D, Thomas, CM, Bannister, JP, & Jaggar, JH. (2010). Isoform-selective physical coupling of TRPC3 channels to IP3 receptors in smooth muscle cells regulates arterial contractility. Circulation Research, 106(10), 1603-1612. PMID: 20378853

Narayanan, D, Xi, Q, Pfeffer, L, & Jaggar, JH. (2010). Mitochondria control functional CaV1.2 expression in smooth muscle cells of cerebral arteries. Circulation Research, 107(5), 631-641. PMID: 20616314 Circulation Research Editors' Pick. Circulation Research Featured Article. Faculty of 1000 Medicine Must Read Article.

Zhao, G, Neeb, Z, Leo, MD, Pachuau, J, Adebiyi, A, Ouyang, K, Chen, J, & Jaggar, JH. (2010). Type 1 IP3 receptors activate BKCa channels via local molecular coupling in arterial smooth muscle cells. Journal of General Physiology, 136(3), 283-291. PMID: 20713546. Journal of General Physiology Journal Club Article by Mujica and González. Selected for Journal of General Physiology Facebook Discussion.

Adebiyi, A, Narayanan, D, & Jaggar, JH. (2011). Caveolin-1 assembles type 1 inositol 1,4,5-trisphosphate receptors and canonical transient receptor potential 3 channels into a functional signaling complex in arterial smooth muscle cells. Journal of Biological Chemistry, 286(6), 4341-4348. PMID: 21098487. Editors Choice: Coupled by Caveolin. Science Signaling, Vol. 4, Issue 160, p. ec50. Featured in NAVBO Publications Alert, March 2011.

Bannister, JP, Thomas-Gatewood, CM, Neeb, ZP, Adebiyi, A, Cheng, X, & Jaggar, JH. (2011). Cav1.2 channel N-terminus splice variants modulate functional surface expression in resistance-size artery smooth muscle cells. Journal of Biological Chemistry, 286(17), 15058-15066. PMID: 21357696. Received Perspective by Joern R Steinert. Journal of Physiology, 2012; 590 (14): 3213-3214.

Bannister JP, Bulley S, Narayanan D, Thomas-Gatewood C, Luzny P, Pachuau J, & Jaggar JH. (2012). Transcriptional upregulation of α2δ-1 elevates arterial smooth muscle cell Cav1.2 channel surface expression and cerebrovascular constriction in genetic hypertension. Hypertension, 60:1006-1015. PMID: 22949532. Commentary by Luis F. Santana and Jose L. Mercado. Hypertension, 2012; 60:894-895.

Bulley S, Neeb ZP, Burris SK, Bannister JP, Thomas-Gatewood CM, Jangsangthong W, & Jaggar JH. (2012). TMEM16A channels contribute to the myogenic response in cerebral arteries. Circulation Research, 111(8):1027-1036. PMID: 22872152.

Adebiyi A, Thomas-Gatewood CM, Leo MD, Kidd MW, Neeb ZP, & Jaggar JH. (2012) An elevation in physical coupling of type 1 IP3 receptors to TRPC3 channels constricts mesenteric arteries in genetic hypertension. Hypertension, 60:1213-1219. PMID: 23045459.

Leo MD, Bannister JP, Narayanan D, Nair A, Grubbs JE, Gabrick KS, Boop FA, Jaggar JH. (2014) Dynamic Regulation of β1 subunit Trafficking Controls Vascular Contractility. Proc Natl Acad Sci USA 111(6):2361-2366. PMID: 24464482.