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LIH CHYUAN NG, Ph.D.
Research Assistant Professor
Ph.D., Strathclyde, Glasgow,
Scotland, 2002
Location: Manville 8B
Email: lng  medicine.nevada.edu
Tel: 775 784-4301
Fax: 775 784-1620
Research Interests
My first research project focused on the role of store-operated calcium entry in hypoxic pulmonary vasoconstriction. Recent study in canine pulmonary artery smooth muscle cells (PASMCs) revealed a rise in [Ca2+]i by hypoxia. The rise in [Ca2+]i induced by hypoxia was contributed by Ca2+ release from the intracellular Ca2+ stores, voltage-operated Ca2+ entry and Ca2+ entry that is insensitive to voltage-operated Ca2+ channels blocker. The dihyropyridine-insensitive rise in [Ca2+]i exhibited pharmacological properties characteristic of capacitative Ca2+ entry (CCE). We conclude that hypoxia activates capacitative Ca2+ entry in canine PASMCs through mobilization of the intracellular Ca2+ stores.
The second project was aimed to characterize the organization of the intracellular Ca2+ stores and the Ca2+ entry pathways activated by store-depletion in cell culture of PASMC. Previous studies have shown that in acutely dispersed PASMCs, IP3- and ryanodine-sensitive Ca2+ stores are functionally independent, and depletion of both stores is required to activate capacitative Ca2+ entry. We found that cell culture of PASMCs results in changes in the organization of Ca2+ stores, with IP3- and ryanodine-sensitive stores being reorganized into a common intracellular compartment and store depletion causes activation of voltage-operated Ca2+ entry and CCE.
My present interest is to determine the molecular identity of store-operated channels that underlie capacitative Ca2+ entry in mouse PASMC. We proposed that TRPC4 could be one of the important TRPC candidates. Experimental techniques include cell culture, Ca2+ imaging, gene and protein expressions, RT-PCR and western blot analysis.
View the publications of Dr Ng on PubMed
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