Jonathan H. Jaggar, Ph.D.

Jaggar photo

Bronstein Endowed Professor of Physiology
847 Monroe Ave
Johnson Building
Memphis, TN 38163

Phone: 901-448-1208
Fax: 901-448-7126


Coventry University, Coventry, UK, B.S. Applied Biology, 
University of Sheffield, Sheffield, UK, 1991-1995, Ph.D., Potassium Channels
University of Vermont, Burlington, VT, 1995-1997, Postdoc., Gastrointestinal Physiology
University of Vermont, Burlington, VT, 1997-1999, Postdoc., Vascular Physiology

Research Interest

My research program investigates physiological functions and pathological alterations in arterial smooth muscle and endothelial cell ion channels. Signaling mechanisms and ion channels that we study include local and global calcium signals, mitochondria, IP3 receptors, voltage-dependent Ca2+ channels, TRP channels, Ca2+-activated Cl- channels, and carbon monoxide and hydrogen sulfide, endogenous physiological gas transmitters.  We also study physiological regulation of ion channel trafficking in arterial smooth muscle cells.  Research in my laboratory incorporates the use of a wide variety of molecular, biochemical, cellular, and functional techniques, including gene knockout and cardiovascular disease models, RT-PCR, Western blotting, biotinylation, FRET, RNAi, co-IP, immunofluorescence, patch-clamp electrophysiology, membrane potential recording, intracellular Ca2+ imaging, arterial myography and blood pressure telemetry.

Representative Publications

    1. Jaggar JH, Li A, Parfenova H, Liu J, Umstot ES, Dopico AM, Leffler CW.  Heme is a carbon monoxide receptor for large-conductance Ca2+-activated K+ channels.  Circ Res 2005; 97 (8): 805-812. PMID: 16166559
    2. Xi Q, Adebiyi A, Zhao G, Chapman KE, Waters CM, Hassid A, Jaggar JH.  IP3 constricts cerebral arteries via IP3 receptor-mediated TRPC3 channel activation and independently of sarcoplasmic reticulum Ca2+ release.  Circ Res 2008; 102(9): 1118-1126. PMID: 18388325
    3. 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.  Circ Res, 105, 948-955.  PMID: 19797702
    4. Adebiyi A, Zhao G, Narayanan D, Thomas-Gatewood CM, Bannister JP, Jaggar JH.  Isoform-selective physical coupling of TRPC3 channels to IP3 receptors in smooth muscle cells regulates arterial contractility.  Circ Res 2010; 106(10): 1603-1612. PMID: 20378853
    5. Narayanan D, Xi Q, Pfeffer L, Jaggar JH.  Mitochondrial control functional Cav1.2 expression in smooth muscle cells of cerebral arteries.  Circ Res 2010; 107(5): 631-641. PMID: 20616314. Circulation Research Featured Article and Editors’ Pick. Faculty of 1000 Medicine Must Read Article.
    6. Adebiyi A, Narayanan D, Jaggar JH.  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.  J Biol Chem 2011; 286 (6): 4341-4348. PMID: 21098487. Editors Choice.  Science Signaling, Vol. 4, Issue 160, p. ec50. Featured in NAVBO Publications Alert, March 2011.
    7. Bulley S, Neeb ZP, Burris SK, Bannister JP, Thomas-Gatewood CM, Jangsangthong W, Jaggar JH.  TMEM16A/ANO1 channels contribute to the myogenic response in cerebral arteries.  Circ Res 2012; 111(8):1027-1036.  PMID: 22872152
    8. 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.
    9. Kidd MW, Leo MD, Bannister JP, Jaggar JH.  Intravascular pressure enhances the abundance of functional Kv1.5 channels at the surface of arterial smooth muscle cells. Science Signaling 2015; 8(390):ra83. doi: 10.1126/scisignal.aac5128. PMID: 26286025.

Additional Information