A functional tandem between transient receptor potential canonical channels 6 and calcium-dependent chloride channels in human epithelial cells

Bertrand, Johanna; Dannhoffer, Luc; Antigny, Fabrice; Vachel, Laura; Jayle, Christophe; Vandebrouck, Clarisse; Becq, Frédéric; Norez, Caroline

doi:10.1016/j.ejphar.2015.08.005

Cited by 12 publications

(9 citation statements)

References 40 publications

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“…Based on the effects of isoform specific TRPC siRNAs, it was suggested that guanabenz may directly activate TRPC6, but not TRPC1. Subsequently, the [Ca 2+ ] c increase evoked by guanabenz causes activation of Ca 2+ -activated Cl − channels in these cells (Bertrand et al, 2015).…”

Section: Modulators For Pulmonary Arterial Hypertension (Pah)-pulmonarymentioning

confidence: 99%

TRPC channels: Structure, function, regulation and recent advances in small molecular probes

Wang

Cheng

Tian

et al. 2020

Pharmacology & Therapeutics

150

152

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Transient receptor potential canonical (TRPC) channels constitute a group of receptor-operated calcium-permeable nonselective cation channels of the TRP superfamily. The seven mammalian TRPC members, which can be further divided into four subgroups (TRPC1, TRPC2, TRPC4/5, and TRPC3/6/7) based on their amino acid sequences and functional similarities, contribute to a broad spectrum of cellular functions and physiological roles. Studies have revealed complexity of their regulation involving several components of the phospholipase C pathway, G i and G o proteins, and internal Ca 2+ stores. Recent advances in cryogenic electron microscopy have provided several high-resolution structures of TRPC channels. Growing evidence demonstrates the involvement of TRPC channels in diseases, particularly the link between genetic mutations of TRPC6 and familial

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Section: Modulators For Pulmonary Arterial Hypertension (Pah)-pulmonarymentioning

confidence: 99%

TRPC channels: Structure, function, regulation and recent advances in small molecular probes

Wang

Cheng

Tian

et al. 2020

Pharmacology & Therapeutics

150

152

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“…Evidence from several laboratories suggested that ClCa could be functionally coupled to plasma membrane Ca 2+ channels [ 165 ]. Interestingly, in human epithelial cells, TRPC6 and ClCa are functionally coupled [ 166 ], and TRPC6 contributes to PH pathogenesis (see Section 3 ). Moreover, in salivary gland cells, TRPC1 is suggested to be essential for the activation of ClCa [ 167 ].…”

Section: Functional and Molecular Classification Of Ion Channels Imentioning

confidence: 99%

Ion Channels in Pulmonary Hypertension: A Therapeutic Interest?

Lambert

Capuano

Olschewski

et al. 2018

IJMS

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Pulmonary arterial hypertension (PAH) is a multifactorial and severe disease without curative therapies. PAH pathobiology involves altered pulmonary arterial tone, endothelial dysfunction, distal pulmonary vessel remodeling, and inflammation, which could all depend on ion channel activities (K+, Ca2+, Na+ and Cl−). This review focuses on ion channels in the pulmonary vasculature and discusses their pathophysiological contribution to PAH as well as their therapeutic potential in PAH.

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“…Functional interplays between TRP cation channels and Ca 2+ -activated chloride channels were so far reported to be mediated by Ca 2+ influx via a number of TRP cation channels, such as TRPC2 45 , TRPC6 46 , and TRPV6 47 . Molecular or physical interaction between TRPs and TMEM16A/ANO1 was also found by Tominaga’s group for TRPV4 48 , 49 and TRPV1 50 .…”

Section: Discussionmentioning

confidence: 99%

TRPM7 is an essential regulator for volume-sensitive outwardly rectifying anion channel

et al. 2021

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Animal cells can regulate their volume after swelling by the regulatory volume decrease (RVD) mechanism. In epithelial cells, RVD is attained through KCl release mediated via volume-sensitive outwardly rectifying Cl− channels (VSOR) and Ca2+-activated K+ channels. Swelling-induced activation of TRPM7 cation channels leads to Ca2+ influx, thereby stimulating the K+ channels. Here, we examined whether TRPM7 plays any role in VSOR activation. When TRPM7 was knocked down in human HeLa cells or knocked out in chicken DT40 cells, not only TRPM7 activity and RVD efficacy but also VSOR activity were suppressed. Heterologous expression of TRPM7 in TRPM7-deficient DT40 cells rescued both VSOR activity and RVD, accompanied by an increase in the expression of LRRC8A, a core molecule of VSOR. TRPM7 exerts the facilitating action on VSOR activity first by enhancing molecular expression of LRRC8A mRNA through the mediation of steady-state Ca2+ influx and second by stabilizing the plasmalemmal expression of LRRC8A protein through the interaction between LRRC8A and the C-terminal domain of TRPM7. Therefore, TRPM7 functions as an essential regulator of VSOR activity and LRRC8A expression.

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A functional tandem between transient receptor potential canonical channels 6 and calcium-dependent chloride channels in human epithelial cells

Cited by 12 publications

References 40 publications

TRPC channels: Structure, function, regulation and recent advances in small molecular probes

TRPC channels: Structure, function, regulation and recent advances in small molecular probes

Ion Channels in Pulmonary Hypertension: A Therapeutic Interest?

TRPM7 is an essential regulator for volume-sensitive outwardly rectifying anion channel

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