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首页> 外文期刊>American Journal of Physiology >Vascular smooth muscle store-operated Ca2+ channels: what a TRP!
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Vascular smooth muscle store-operated Ca2+ channels: what a TRP!

机译：血管平滑肌存储操作的Ca2 +通道：真是一个TRP！

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calcium entry triggered by loss of Ca~(+) from endoplasmic reticulum Ca~(+) stores in vascular smooth muscle cells was first described by Casteels and Droogmans (6) 25 years ago. Subsequent studies have demonstrated that this is a ubiquitous process occurring in all eukaryotes from yeast to humans (see recent reviews for details: Refs. 4, 21, 31). However, the molecular identity of the ion channels that underlie store-operated Ca~(+) (SOC) entry remains one of the significant unanswered questions in this important area of research. Compelling evidence has been presented that members of the canonical transient receptor potential family of channels, particularly TRPC1, are involved in SOC entry in vascular smooth muscle cells (5, 11, 28, 33) and in other cell types (see Ref. 21 for numerous references). However, it is also clear that TRPC1 alone is unlikely to represent the SOC channel (SOCC) expressed in these cells (4, 21). The study by Xu et al. (34) in this issue of the American Journal of Physiology, Heart and Circulatory Physiology, confirms and extends a preliminary report by this same group (35) that TRPC5 is another component of vascular smooth muscle SOCC. These findings are important for at least two reasons. First, the identity of an additional component of SOC entry in native vascular smooth muscle cells is a significant advance in our understanding of this important area of research. While TRP channels long have been implicated as SOCC, the characteristics of channels formed by individual TRP channel isoforms have poorly matched the characteristics of SOCC expressed in native cells. As demonstrated by Xu and colleagues (34, 35), the whole cell currents, ion selectivity, and pharmacology of SOCC in rabbit cerebral arteriolar smooth muscle cells nicely match heterolo-gously expressed TRPC1/TRPC5 heteromultimers, strongly supporting a role for both TRPC isoforms in SOC entry in this system. However, it also should be noted that the hypothesis that TRPC1/TRPC5 heteromers represent at least a component of SOCC in native vascular smooth muscle cells has not been critically tested (see below)
机译：25年前，Casteels和Droogmans（6）首先描述了内质网中Ca〜（+）从内质网中Ca〜（+）的丢失触发的钙进入。随后的研究表明，这是从酵母到人类的所有真核生物中普遍存在的过程（有关详细信息，请参见最新评论：参考文献4、21、31）。然而，作为存储操作的Ca〜（+）（SOC）条目基础的离子通道的分子同一性，仍然是这一重要研究领域中尚未解决的重要问题之一。已有令人信服的证据表明，规范瞬时受体潜在通道家族的成员，尤其是TRPC1，参与了血管平滑肌细胞（5、11、28、33）和其他细胞类型的SOC进入（参见参考文献21）。大量参考文献）。但是，也很清楚，单独的TRPC1不太可能代表这些细胞中表达的SOC通道（SOCC）（4，21）。徐等人的研究。 [34]在《美国生理，心脏和循环生理学杂志》上，证实并延伸了同一组研究的初步报告（35），认为TRPC5是血管平滑肌SOCC的另一个组成部分。这些发现很重要，至少有两个原因。首先，在天然血管平滑肌细胞中SOC进入的其他成分的识别是我们对这一重要研究领域的理解的重大进步。尽管长期以来一直将TRP通道与SOCC牵连，但由单个TRP通道同工型形成的通道的特性与天然细胞中表达的SOCC的特性很难匹配。正如Xu及其同事（34，35）所证明的，兔脑小动脉平滑肌细胞中的全细胞电流，离子选择性和SOCC的药理学很好地匹配了异源表达的TRPC1 / TRPC5异源多聚体，强烈支持了这两种TRPC亚型的作用在此系统中的SOC条目中。但是，还应注意，尚未对TRPC1 / TRPC5异聚体至少代表天然血管平滑肌细胞中SOCC的成分这一假说进行过严格检验（见下文）。

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