NYMC > Faculty > Directory > By Name > Wang, Wenhui

Wenhui Wang, M.D.

Professor of Pharmacology

E-mail:  wenhui_wang@nymc.edu

Phone: (914) 594-4139/4120/4737

Address:

Department of Pharmacology
Basic Science Building, Rm. 527A
15 Dana Road
Valhalla, NY  10595

Research Interests:

My laboratory is focused on studying the regulation of Na+ and K+ transport in aldosterone-sensitive distal tubules of the kidney. Na+ is a major extracellular ion and plays a key role in maintaining extracellular volume, and decreasing extracellular Na+ content can result in hypotension whereas increasing Na+ content causes hypertension. Conversely, K+ is mainly located in the intracellular fluid and extracellular K+ must be maintained in a narrow range: either high plasma K+ (hyperkalemia) or low plasma K+ (hypokalemia) can cause life-threatening cardiac arrhythmias. The kidney plays a key role in secreting K+ to match the dietary K+ intake, and disorders of K+ balance are common in patients with kidney failure.

We have two research projects funded by the National Institutes of Health.

Regulation and Modulation of Renal K+ channels in Kidney:

Molecular, biochemical and electrophysiological approaches are being used to study the molecular mechanisms involved in the regulation of renal K+ channels. We have found that protein tyrosine kinases and WNK+ (with-no-lysine kinase) play an important role in the regulation of renal K+ secretion. Using miRNA+ array we have also identified several miRNA+ that regulate renal K+ channels - these include miR-802, miR-192 and miR142-3P.

Regulation of Epithelial Na+ Channels by epoxyeicosatrienoic acids (EETs):

Arachidonic acid can be metabolized to EETs by the cytochrome P450 epoxygenase CYP2C44, and we have found that EETs play an important role in the regulation of Na+ transport in the distal nephron. High Na+ intake stimulates CYP2C44 activity and thus inhibits Na+ absorption in the distal nephron, and defective regulation of CYP2C44 can cause the salt-sensitive hypertension. We are currently using genetically modified mice to study the role of CYP2C44 in regulating epithelial Na+ channels in the kidney.

Selected Publications in the Last 5 years:

  1. Dimin Li, Zhijian Wang, Peng Sun, Yan Jin, Dao-Hong Lin, Steven C. Hebert, Gerhard Giebisch and Wen-Hui Wang. Inhibition of MAPK+ stimulates the Ca2+-dependent big-conductance K+ channels in cortical collecting duct. PNAS 103;19569-19574, 2006.
  2. Yuan Wei, Beth Zavilowitz, Lisa M. Satlin, and Wen-Hui Wang. Angiotensin II Inhibits the ROMK-like Small Conductance K+ Channel in Renal Cortical Collecting Duct during Dietary Potassium Restriction, J. Bio. Chem., 282:6455-6462, 2006.
  3. Peng Sun, Wen Liu, Dao-Hong Lin, Peng Yue, Rowena Kemp, Lisa M. Satlin, and Wen-Hui Wang.  Epoxyeicosatrienoic Acid Activates BK+ Channels in the Cortical Collecting Duct, J Am Soc Nephrol 20: 513–523, 2009.
  4. Peng Yue, Dao-Hong Lin, Chun-Yang Pan, Qiang Leng, Gerhard Giebisch, Richard P. Lifton, and Wen-Hui Wang, Src family protein tyrosine kinase (PTK) modulates the effect of SGK1 and WNK4 on ROMK+ channels. PNAS . 106: 15061–15066, 2009
  5. Dao-Hong Lin, Peng Yue, Chu-Yang Pan, Peng Sun, Xin Zhang, Zeguang Han, Marcel Roos, Michael Caplan, Gerhard Giebisch, and Wen-Hui Wang. POSH Stimulates the Ubiquitination and the Clathrin-independent Endocytosis of ROMK1 Channels. J. Biol. Chem. 284: 29614–29624, 2009.
  6. Chen, Y-J, Li, Jing and Quilley, J. Deficient renal 20-HETE release in the diabetic rat is not the result of oxidative stress. Am. J. Physiol. 294:H2305-H2312, 2008.

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