Jonathan H. Jaggar, Ph.D.

Jonathan H. Jaggar, Ph.D.

Maury Bronstein Professor
Department of Physiology


The University of Tennessee Health Science Center
894 Union Avenue
Memphis, TN 38163
Phone: (901) 448-1208
Office: 402 Nash Research Building
Email: Jonathan H. Jaggar


Education

  • Ph.D. Institution: University of Sheffield, United Kingdom

Research Interests

Arterial diameter, a primary determinant of systemic blood pressure, is regulated by the contractile state of smooth muscle cells in the arterial wall. One critical regulator of smooth muscle contractility is the intracellular calcium ion concentration. Smooth muscle cells control intracellular calcium concentration by regulating cellular influx, release, sequestration and extrusion. Since membrane potential regulates calcium entry in smooth muscle cells, ion channels that modulate membrane potential also change cellular contractility. Recent studies have discovered that local and global elevations in cytosolic calcium occur in smooth muscle cells. These different calcium signaling events not only regulate contractility, but may also regulate a number of other physiological functions. We are currently investigating sarcolemma ion channels that control membrane potential and calcium entry in arterial smooth muscle cells and the properties, physiological targets, and regulation of arterial diameter by different intracellullar calcium signals. Research in the laboratory involves a multi-faceted approach, studying events at molecular, cellular and intact artery levels. Techniques include patch clamp electrophysiology, rapid confocal calcium imaging, conventional calcium imaging, diameter measurement of pressurized arteries, and molecular biology.

Representative Publications

  • Zhai X, Leo MD, Jaggar JH. Endothelin-1 Stimulates Vasoconstriction Through Rab11A Serine 177 Phosphorylation. Circ Res. 2017 Sep 1;121(6):650-661. doi: 10.1161/CIRCRESAHA.117.311102. Epub 2017 Jul 10. PubMed PMID: 28696251; PubMed Central PMCID: PMC5581242.
  • Leo MD, Zhai X, Muralidharan P, Kuruvilla KP, Bulley S, Boop FA, Jaggar JH. Membrane depolarization activates BK channels through ROCK-mediated β1 subunit surface trafficking to limit vasoconstriction. Sci Signal. 2017 May 9;10(478). pii: eaah5417. doi: 10.1126/scisignal.aah5417. PubMed PMID: 28487419.
  • Jaggar JH, VanHook AM. Science Signaling Podcast for 9 May 2017: Trafficking of BK channel subunits in arterial myocytes. Sci Signal. 2017 May 9;10(478). pii: eaan4849. doi: 10.1126/scisignal.aan4849. PubMed PMID: 28487418.
  • Hasan R, Leeson-Payne ATS, Jaggar JH, Zhang X. Corrigendum: Calmodulin is responsible for Ca(2+)-dependent regulation of TRPA1 Channels. Sci Rep. 2017 May 4;7:46588. doi: 10.1038/srep46588. PubMed PMID: 28471425; PubMed Central PMCID: PMC5417011.
  • Hasan R, Leeson-Payne AT, Jaggar JH, Zhang X. Calmodulin is responsible for Ca(2+)-dependent regulation of TRPA1 Channels. Sci Rep. 2017 Mar 23;7:45098. doi: 10.1038/srep45098. PubMed PMID: 28332600; PubMed Central PMCID: PMC5362816.
  • Kidd MW, Bulley S, Jaggar JH. Angiotensin II reduces the surface abundance of K(V) 1.5 channels in arterial myocytes to stimulate vasoconstriction. J Physiol. 2017 Mar 1;595(5):1607-1618. doi: 10.1113/JP272893. Epub 2017 Feb 5. PubMed PMID: 27958660; PubMed Central PMCID: PMC5330887.

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