Swapnil Sonkusare

Sonkusare, Swapnil

Primary Appointment

Assistant Professor, Molecular Physiology and Biological Physics

Education

  • PhD, Pharmacology, University of Arkansas for Medical Sciences
  • Postdoc, Vascular ion channels, University of Vermont

Contact Information

409 Lane Road
MR4 Toom 6051A
Charlottesville, VA 22901
Telephone: 434-297-7401
Email: sks2n@virginia.edu
Website: http://www.cvrc.virginia.edu/Sonkusare/index.html

Research Disciplines

Biophysics, Cardiovascular Biology, Physiology

Research Interests

Microcirculation, vascular ion channels, calcium signaling mechanisms, endothelial cells, hypertension

Research Description

Endothelial cells line the inner walls of all the arteries, where they release substances that can cause vasodilation and lower the blood pressure. The loss of endothelium-dependent vasodilation increases vascular resistance and blood pressure in cardiovascular disorders. Thus, strategies to target the loss of endothelium-dependent vasodilation may have therapeutic benefit in cardiovascular disorders.

Under normal conditions, endothelium-dependent vasodilation is driven by increases in intracellular calcium. My laboratory studies the activity of individual calcium entry events in endothelial cells and their signaling targets under normal and disease conditions. We focus on two life-threatening disorders that are commonly associated with the loss of endothelial function- obesity and pulmonary hypertension. New findings reveal that calcium influx through TRPV4 ion channels, a key calcium entry pathway in endothelial cells, is drastically reduced in rodent models of obesity or pulmonary hypertension and in human patients. The overarching goal is to rescue TRPV4 ion channel activity in obesity and pulmonary hypertension by specifically targeting the causative mechanisms that lower TRPV4 ion channel activity. Our current studies attempt to improve the interaction between TRPV4 ion channels and their regulatory proteins (AKAP150 in systemic circulation and caveolin-1 in pulmonary circulation) in order to enhance endothelium-dependent vasodilation and decrease vascular resistance.

We use a combination of state-of-the-art techniques to achieve a comprehensive understanding of calcium signaling mechanisms that control vascular resistance, including high-speed confocal imaging of calcium signals, patch clamp electrophysiology to measure ion channel currents, and measurements of arterial diameter and blood pressure coupled with several transgenic mouse models.

Selected Publications