TRPC1 functions as a store-operated Ca<sup>2+</sup>channel in intestinal epithelial cells and regulates early mucosal restitution after wounding

Rao, Jaladanki N.; Platoshyn, Oleksandr; Golovina, Vera A.; Liu, Lan; Zou, Tongtong; Marasa, Bernard S.; Turner, Douglas J.; Yuan, Jason X.‐J.; Wang, Jian Ying

doi:10.1152/ajpgi.00441.2005

Cited by 109 publications

(127 citation statements)

References 58 publications

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“…The repopulation of the cell-free "wound" area is primarily due to astrocyte proliferation, although migration does also contribute to this process (Környei et al, 2000). A role of SOCE in wound closure has been proposed previously (Rao et al, 2006). Our study strongly suggests that mitochondrial Ca 2ϩ transfer through NCLX is essential to facilitate SOCE, and therefore may affect astrocytic proliferation and the regrowth of the astrocytes into the denuded areas of the wound.…”

Section: Nclx Activity Differentially Affects Migration/proliferationsupporting

confidence: 76%

Mitochondrial Exchanger NCLX Plays a Major Role in the Intracellular Ca²⁺Signaling, Gliotransmission, and Proliferation of Astrocytes

et al. 2013

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Section: Nclx Activity Differentially Affects Migration/proliferationsupporting

confidence: 76%

Mitochondrial Exchanger NCLX Plays a Major Role in the Intracellular Ca²⁺Signaling, Gliotransmission, and Proliferation of Astrocytes

et al. 2013

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“…A detailed review critically reevaluates the role of TRP channels as mechanosensitive channels [39]. Nonetheless, a function of TRPC1 has been shown in the migration of intestinal epithelial cells during closure of a wounded epithelial layer [32]. In the present study, we investigated the role of the putative mechanosensitive Ca 2+ channel TRPC1 in single-cell migration of MDCK-F cells.…”

Section: Introductionmentioning

confidence: 94%

TRPC1 channels regulate directionality of migrating cells

Fabian

Fortmann

Dieterich

et al. 2008

Pflugers Arch - Eur J Physiol

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Cell migration depends on the generation of structural asymmetry and on different steps: protrusion and adhesion at the front and traction and detachment at the rear part of the cell. The activity of Ca 2+ channels coordinate these steps by arranging intracellular Ca 2+ signals along the axis of movement. Here, we investigated the role of the putative mechanosensitive canonical transient receptor potential channel 1 (TRPC1) in cell migration. We analyzed its function in transformed renal epithelial (Madin-Darby canine kidney-focus) cells with variation of TRPC1 expression. As shown by time lapse video microscopy, TRPC1 knockdown cells have partially lost their polarity and the ability to persistently migrate into a given direction. This failure is linked to the suppression of a local Ca 2+ gradient at the front of migrating TRPC1 knockdown cells, whereas TRPC1 overexpression leads to steeper Ca 2+ gradients. We propose that the Ca 2+ signaling events regulated by TRPC1 within the lamellipodium determine polarity and directed cell migration.

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“…This cell line was developed and characterized initially by Suh and Traber [30], and then characterized further by others [23,31,32]. The forced expression of the Cdx2 gene in IEC-6 cells results in development of a differentiated phenotype [23,31].…”

Section: Cell Culturementioning

confidence: 99%

Depolarization and decreased surface expression of K+ channels contribute to NSAID-inhibition of intestinal restitution

Freeman

Narváez

McCoy

et al. 2007

Biochemical Pharmacology

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Non-steroidal anti-inflammatory drugs (NSAIDs) contribute to gastrointestinal ulcer formation by inhibiting epithelial cell migration and mucosal restitution; however, the drug-affected signaling pathways are poorly defined. We investigated whether NSAID inhibition of intestinal epithelial migration is associated with depletion of intracellular polyamines, depolarization of membrane potential (E m ) and altered surface expression of K + channels. Epithelial cell migration in response to the wounding of confluent IEC-6 and IEC-Cdx2 monolayers was reduced by indomethacin (100 μM), phenylbutazone (100 μM) and NS-398 (100 μM) but not by SC-560 (1 μM). NSAIDinhibition of intestinal cell migration was not associated with depletion of intracellular polyamines. Treatment of IEC-6 and IEC-Cdx2 cells with indomethacin, phenylbutazone and NS-398 induced significant depolarization of E m , whereas treatment with SC-560 had no effect on E m . The E m of IEC-Cdx2 cells was: −38.5±1.8 mV under control conditions; −35.9±1.6 mV after treatment with SC-560; −18.8±1.2 mV after treatment with indomethacin; and −23.7±1.4 mV after treatment with NS-398. Whereas SC-560 had no significant effects on the total cellular expression of K v 1.4 channel protein, indomethacin and NS-398 decreased not only the total cellular expression of K v 1.4, but also the cell surface expression of both K v 1.4 and K v 1.6 channel subunits in IEC-Cdx2. Both K v 1.4 and K v 1.6 channel proteins were immunoprecipitated by K v 1.4 antibody from IEC-Cdx2 lysates, indicating that these subunits co-assemble to form heteromeric K v channels. These results suggest that NSAID inhibition of epithelial cell migration is independent of polyamine-depletion, and is associated with depolarization of E m and decreased surface expression of heteromeric K v 1 channels.

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TRPC1 functions as a store-operated Ca²⁺channel in intestinal epithelial cells and regulates early mucosal restitution after wounding

Abstract: . TRPC1 functions as a store-operated Ca 2ϩ channel in intestinal epithelial cells and regulates early mucosal restitution after wounding.

Cited by 109 publications

References 58 publications

Mitochondrial Exchanger NCLX Plays a Major Role in the Intracellular Ca²⁺Signaling, Gliotransmission, and Proliferation of Astrocytes

Mitochondrial Exchanger NCLX Plays a Major Role in the Intracellular Ca²⁺Signaling, Gliotransmission, and Proliferation of Astrocytes

TRPC1 channels regulate directionality of migrating cells

Depolarization and decreased surface expression of K+ channels contribute to NSAID-inhibition of intestinal restitution

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TRPC1 functions as a store-operated Ca2+channel in intestinal epithelial cells and regulates early mucosal restitution after wounding

Abstract: . TRPC1 functions as a store-operated Ca 2ϩ channel in intestinal epithelial cells and regulates early mucosal restitution after wounding.

Cited by 109 publications

References 58 publications

Mitochondrial Exchanger NCLX Plays a Major Role in the Intracellular Ca2+Signaling, Gliotransmission, and Proliferation of Astrocytes

Mitochondrial Exchanger NCLX Plays a Major Role in the Intracellular Ca2+Signaling, Gliotransmission, and Proliferation of Astrocytes

TRPC1 channels regulate directionality of migrating cells

Depolarization and decreased surface expression of K+ channels contribute to NSAID-inhibition of intestinal restitution

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TRPC1 functions as a store-operated Ca²⁺channel in intestinal epithelial cells and regulates early mucosal restitution after wounding

Mitochondrial Exchanger NCLX Plays a Major Role in the Intracellular Ca²⁺Signaling, Gliotransmission, and Proliferation of Astrocytes

Mitochondrial Exchanger NCLX Plays a Major Role in the Intracellular Ca²⁺Signaling, Gliotransmission, and Proliferation of Astrocytes