Increased Vascular Smooth Muscle Contractility in <i>TRPC6</i><sup>−/−</sup> Mice

Dietrich, Alexander; Schnitzler, Michael Mederos y; Gollasch, Maik; Groß, Volkmar; Storch, Ursula; Dubrovska, Galyna; Obst, Michael; Yildirim, E.; Salanova, Birgit; Essin, Kirill; Pinkenburg, Olaf; Luft, Friedrich C.; Gudermann, Thomas; Birnbaumer, Lutz

doi:10.1128/mcb.25.24.11191.2005

Cited by 126 publications

(216 citation statements)

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“…However, we consider this unlikely for the following reasons. Previous analysis of the TRPC1 −/− mouse vasculature suggested that there is no upregulation or downregulation of other TRPC channels [23], unlike the situation in TRPC6 −/− mice where TRPC3 levels are elevated [27]. We have found that levels of TRPC6 in wild-type versus TRPC1 −/− platelets are unchanged (Fig.…”

Section: Discussionmentioning

confidence: 46%

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Store-operated Ca2+ entry in platelets occurs independently of transient receptor potential (TRP) C1

Varga-Szabó

Authi

Braun

et al. 2008

Pflugers Arch - Eur J Physiol

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Changes in [Ca 2+ ] i are a central step in platelet activation. In nonexcitable cells, receptor-mediated depletion of intracellular Ca 2+ stores triggers Ca 2+ entry through store-operated calcium (SOC) channels. Stromal interaction molecule 1 (STIM1) has been identified as an endoplasmic reticulum (ER)-resident Ca 2+ sensor that regulates storeoperated calcium entry (SOCE), but the identity of the SOC channel in platelets has been controversially debated. Some investigators proposed transient receptor potential (TRP) C1 to fulfil this function based on the observation that antibodies against the channel impaired SOCE in platelets. However, others could not detect TRPC1 in the plasma membrane of platelets and raised doubts about the specificity of the inhibiting anti-TRPC1 antibodies. To address the role of TRPC1 in SOCE in platelets, we analyzed mice lacking TRPC1. Platelets from these mice display fully intact SOCE and also otherwise unaltered calcium homeostasis compared to wild-type. Furthermore, platelet function in vitro and in vivo is not altered in the absence of TRPC1. Finally, studies on human platelets revealed that the presumably inhibitory anti-TRPC1 antibodies have no specific effect on SOCE and fail to bind to the protein. Together, these results provide evidence that SOCE in platelets is mediated by channels other than TRPC1.

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Section: Discussionmentioning

confidence: 46%

“…1c). Platelets from TRPC6 −/− mice [27] served as a control. To estimate store content and SOCE in the cells, we performed intracellular Ca 2+ measurements.…”

Section: Resultsmentioning

confidence: 99%

Store-operated Ca2+ entry in platelets occurs independently of transient receptor potential (TRP) C1

Varga-Szabó

Authi

Braun

et al. 2008

Pflugers Arch - Eur J Physiol

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“…TRPC6 -/-mice are characterized by high blood pressure, increased contractility of isolated aortic rings in response to agonists, and enhanced MR in cerebral arteries [50]. However, the level of TRPC3 expression is much higher in arterial myocytes from TRPC6 −/− mice.…”

Section: Sacsmentioning

confidence: 99%

“…However, the level of TRPC3 expression is much higher in arterial myocytes from TRPC6 −/− mice. These smooth muscle cells are more depolarized and show a higher basal cation entry [50]. Elimination of this current by TRPC3-specific siRNA indicates that TRPC3 channels are upregulated in TRPC6 −/− mice, leading to vasoconstriction [50].…”

Section: Sacsmentioning

confidence: 99%

“…These smooth muscle cells are more depolarized and show a higher basal cation entry [50]. Elimination of this current by TRPC3-specific siRNA indicates that TRPC3 channels are upregulated in TRPC6 −/− mice, leading to vasoconstriction [50]. To avoid this compensatory gene remodeling, a TRPC6 antisense oligonucleotide strategy has been used in isolated cultured arteries.…”

Section: Sacsmentioning

confidence: 99%

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Canonical TRP channels and mechanotransduction: from physiology to disease states

Patel

Sharif‐Naeini

Folgering

et al. 2010

Pflugers Arch - Eur J Physiol

133

105

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Mechano-gated ion channels play a key physiological role in cardiac, arterial, and skeletal myocytes. For instance, opening of the non-selective stretch-activated cation channels in smooth muscle cells is involved in the pressure-dependent myogenic constriction of resistance arteries. These channels are also implicated in major pathologies, including cardiac hypertrophy or Duchenne muscular dystrophy. Seminal work in prokaryotes and invertebrates highlighted the role of transient receptor potential (TRP) channels in mechanosensory transduction. In mammals, recent findings have shown that the canonical TRPC1 and TRPC6 channels are key players in muscle mechanotransduction. In the present review, we will focus on the functional properties of TRPC1 and TRPC6 channels, on their mechano-gating, regulation by interacting cytoskeletal and scaffolding proteins, physiological role and implication in associated diseases.

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Low‐glucose‐sensitive TRPC6 dysfunction drives hypoglycemia‐induced cognitive impairment in diabetes

Gao

Cui

et al. 2020

Clinical & Translational Med

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Increased Vascular Smooth Muscle Contractility in TRPC6^−/− Mice

Cited by 126 publications

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Store-operated Ca2+ entry in platelets occurs independently of transient receptor potential (TRP) C1

Store-operated Ca2+ entry in platelets occurs independently of transient receptor potential (TRP) C1

Canonical TRP channels and mechanotransduction: from physiology to disease states

Low‐glucose‐sensitive TRPC6 dysfunction drives hypoglycemia‐induced cognitive impairment in diabetes

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Increased Vascular Smooth Muscle Contractility in TRPC6−/− Mice

Cited by 126 publications

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Store-operated Ca2+ entry in platelets occurs independently of transient receptor potential (TRP) C1

Store-operated Ca2+ entry in platelets occurs independently of transient receptor potential (TRP) C1

Canonical TRP channels and mechanotransduction: from physiology to disease states

Low‐glucose‐sensitive TRPC6 dysfunction drives hypoglycemia‐induced cognitive impairment in diabetes

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Increased Vascular Smooth Muscle Contractility in TRPC6^−/− Mice