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TRPC1 is required for directed cell migration
Author(s) -
Fabian Anke,
Fortmann Thomas,
Dieterich Peter,
Schön Peter,
Riethmüller Christoph,
Mally Sabine,
Schwab Albrecht
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.2_supplement.79
Subject(s) - mechanosensitive channels , trpc1 , microbiology and biotechnology , chemotaxis , cell migration , polarity (international relations) , cell , cell polarity , biology , chemistry , ion channel , receptor , biochemistry
Lamellipodial protrusion and directed cell migration depends on cellular asymmetry and the arrangement of forces generated in different regions of the cell. Fine‐tuned cytosolic Ca 2+ signals that are critical for coordinating theses forces originate among others from stretch‐activated Ca 2+ channels. Currently, the molecular identity of such channels is under debate. We investigated the role of the putative mechanosensitive TRPC1 channel in cell migration. We analyzed its function in transformed renal epithelial (MDCK‐F) cells with variations of TRPC1 channel expression. TRPC1 depleted cells have broad protrusions into several directions simultaneously and a partial loss of cellular polarity. Besides their remarkable morphological change these cells show reduced persistence in migration, diminished translocations and no chemotaxis towards FGF‐2 as analyzed by time‐lapse video microscopy. In line with this, pharmacological inhibition of TRPC1 with the venom GsMTx‐4 impairs chemotaxis as well as random movement. Taken together our data suggest that the putative mechanosensitive Ca 2+ channel TRPC1 controls cell polarity and has strong impact on directed cell migration.