TRP Channels

TRP Channels

New Book on TRP Channels

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Transient Receptor Potential Channels offers a unique blend of thoughtfully selected topics ranging from the structural biology of this fascinating group of ion channels to their emerging roles in human diseases. This single book covers TRP channels of yeasts, flies, fishes frogs and humans. And from the biophysics of primary thermo-sensory events in cells to the thermosensation at whole organism level, from physiology of pain to the development of pain-killers, from psychiatric illnesses to cancers, from skin cells to sperms, from taste buds to testes, from established facts to heated debates, this book contains something for every TRP enthusiasts, beginner and expert alike. It includes crucial background information, critical analysis of cutting edge research, and ideas and thoughts for numerous testable hypotheses. It also shows directions for future research in this highly dynamic field. It is a book readers will be just as eager to give to others as keep for themselves. Transient Receptor Potential Channels (Advances in Experimental Medicine and Biology) [Hard cover]. Md. Shahidul Islam (Editor). Publisher: Springer. 52 chapters, 125 authors, about 1115 pages

Chapter 38

AbstractsPosted by Md. Shahidul Islam Mon, January 31, 2011 22:14:32

Molecular Expression and Functional Role of Canonical Transient Receptor Potential Channels in Airway Smooth Muscle Cells

Yong-Xiao Wang and Yun-Min Zheng

Multiple canonical or classic transient receptor potential (TRPC) molecules are expressed in animal and human airway smooth muscle cells (SMCs). TRPC3, but not TRPC1, is a major molecular component of native non-selective cation channels (NSCCs) to contribute to the resting [Ca2+]i and muscarinic increase in [Ca2+]i in freshly isolated airway SMCs. TRPC3-encoded NSCCs are significantly increased in expression and activity in airway SMCs from ovalbuminsensitized/challenged "asthmatic" mice, whereas TRPC1-encoded channel activity, but not its expression, is largely augmented. The upregulated TRPC3- and TRPC1-encoded NSCC activity both mediate "asthmatic" membrane depolarization in airway SMCs. Supportively, tumor necrosis factor-α (TNFα), an important asthma mediator, increases TRPC3 expression, and TRPC3 gene silencing inhibits TNFα-mediated augmentation of acetylcholine-evoked increase in [Ca2+]i in passaged airway SMCs. In contrast, TRPC6 gene silencing has no effect on 1-oleoyl-2-acetylsn-glycerol (OAG)-evoked increase in [Ca2+]i in primary isolated cells. These findings provide compelling information indicating that TRPC3-encoded NSCCs are important for physiological and pathological cellular responses in airway SMCs. However, continual studies are necessary to further determine whether, which, and how TRPC-encoded channels are involved in cellular responses in normal and diseased (e.g., asthmatic) airway SMCs.

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