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TRPC Family of Ion Channels and Mechanotransduction

  • Chapter
Sensing with Ion Channels

Part of the book series: Springer Series in Biophysics ((BIOPHYSICS,volume 11))

Here we review recent evidence that indicates members of the canonical transient receptor potential (TRPC) channel family form mechanosensitive (MS) channels. The MS functions of TRPCs may be mechanistically related to their better known functions as store-operated (SOCs) and receptor-operated channels (ROCs). In particular, mechanical forces may be conveyed to TRPC channels through “conformational coupling” and/or “Ca2+ influx factor” mechanisms that are proposed to transmit information regarding the status of internal Ca2+ stores to SOCs located in the plasma membrane. Furthermore, all TRPCs are regulated by receptors coupled to phospholipases (e.g., PLC and PLA2) that may themselves display mechanosensitivity and modulate channel activity via their generation of lipidic second messengers (e.g., diacylglycerol, lysophospholipids and arachidonic acid). Accordingly, there may be several nonexclusive mechanisms by which mechanical forces may regulate TRPC channels, including direct sensitivity to bilayer deformations (e.g., involving changes in lipid packing, bilayer thickness and/or lateral pressure profile), physical coupling to internal membranes and/or cytoskeletal proteins, and sensitivity to lipidic second messengers generated by MS enzymes. Various strategies that can be used to separate out different MS gating mechanisms and their possible role in each of the TRPCs are discussed.

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  1. Department of Neuroscience and Cell Biology, University of Texas Medical Branch, 77555, Galveston, TX, USA

    Owen P. Hamill & Rosario Maroto

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  1. Owen P. Hamill
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  2. Rosario Maroto
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  1. University of Queensland, Qld 4072, Brisbane, Australia

    Boris Martinac

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Hamill, O.P., Maroto, R. (2008). TRPC Family of Ion Channels and Mechanotransduction. In: Martinac, B. (eds) Sensing with Ion Channels. Springer Series in Biophysics, vol 11. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-540-72739-2_7

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