James Sham, PhD
Highlights
Languages
- English
Gender
MaleJohns Hopkins Affiliations:
- Johns Hopkins School of Medicine Faculty
About James Sham
Primary Academic Title
Professor of Medicine
Background
Dr. James Sham is a Professor of Medicine at the Johns Hopkins University School of Medicine. He received his bachelor and master degrees from the Chinese University of Hong Kong, and his PhD degree from the Johns Hopkins University. He completed postdoctoral fellowship at the University of Pennsylvania before joining the Johns Hopkins faculty.
Contact for Research Inquiries
5501 Hopkins Bayview Circle
Room 5B.43
Baltimore, MD 21224
Phone: (410) 550-7751
Fax: (410) 550-2612
jsks@jhmi.edu
Research Interests
Calcium regulation in chronic hypoxic pulmonary hypertension, Local calcium signaling in the pulmonary arteries, TRP channels in pulmonary arterial smooth muscle cells
Lab Website
James Sham Lab
- Research in the James Sham Lab focuses on pulmonary arteries. Studies include local calcium signaling in the pulmonary arteries and transient receptor potential (TRP) channels in pulmonary arterial smooth muscle cells. We're also interested in calcium regulation in chronic hypoxic pulmonary hypertension.
Research Summary
Dr. Sham is a cellular physiologist and his research is focused on Ca2+ signaling and regulation of ion channels in pulmonary vasculature and cardiovascular systems. His laboratory was among the first to provide the experimental evidence for the functional coupling between the L-type Ca2+ channel and ryanodine receptors in cardiac myocytes; and to examine local Ca2+ fluxes or “Ca2+ spikes” in the dyadic junction to study the mechanisms underlying ryanodine-dependent Ca2+ release activation and termination. His current research interest includes: (1) Local Ca2+ events and cross-talk between ryanodine receptors and IP3 receptors of sarcoplasmic reticulum and NAADP-gated Ca2+ stores (acidic lysosomal Ca2+ stores) in pulmonary arterial smooth muscle cells; (2) the physiological functions and regulation of transient receptor potential (TRPC, TRPM, and TRPV) channels in pulmonary vasculatures; and (3) the pathological alterations of Ca2+ signaling in pulmonary vascular cells and their contributions to pulmonary hypertension. Recently, he is also interested in the ionic mechanisms of carotid body activation related to obesity or leptin-dependent hypertension.