通过储存式钙内流对外分泌腺上皮离子转运的调节。
Regulation of epithelial ion transport in exocrine glands by store-operated Ca entry.
作者信息
Concepcion Axel R, Feske Stefan
机构信息
Department of Pathology, New York University School of Medicine, New York, NY, 10016, USA.
Department of Pathology, New York University School of Medicine, New York, NY, 10016, USA.
出版信息
Cell Calcium. 2017 May;63:53-59. doi: 10.1016/j.ceca.2016.12.004. Epub 2016 Dec 21.
Store-operated Ca entry (SOCE) is a conserved mechanism of Ca influx that regulates Ca signaling in many cell types. SOCE is activated by depletion of endoplasmic reticulum (ER) Ca stores in response to physiological agonist stimulation. After it was first postulated by J.W. Putney Jr. in 1986, SOCE has been described in a large number of non-excitable cell types including secretory cells of different exocrine glands. Here we discuss the mechanisms by which SOCE controls salt and fluid secretion in exocrine glands, with a special focus on eccrine sweat glands. In sweat glands, SOCE plays an important, non-redundant role in regulating the function of Ca-activated Cl channels (CaCC), Cl secretion and sweat production. In the absence of key regulators of SOCE such as the CRAC channel pore subunit ORAI1 and its activator STIM1, the Ca-activated chloride channel TMEM16A is inactive and fails to secrete Cl, resulting in anhidrosis in mice and human patients.
储存性钙内流（SOCE）是一种保守的钙内流机制，可调节多种细胞类型中的钙信号传导。SOCE通过内质网（ER）钙库的耗竭而被激活，以响应生理激动剂刺激。自1986年由小J.W.普特尼首次提出以来，SOCE已在大量非兴奋性细胞类型中得到描述，包括不同外分泌腺的分泌细胞。在这里，我们讨论SOCE控制外分泌腺中盐和液体分泌的机制，特别关注小汗腺。在汗腺中，SOCE在调节钙激活氯离子通道（CaCC）的功能、氯离子分泌和汗液产生方面发挥着重要的、不可替代的作用。在缺乏SOCE的关键调节因子（如CRAC通道孔亚基ORAI1及其激活剂STIM1）的情况下，钙激活氯离子通道TMEM16A失活，无法分泌氯离子，导致小鼠和人类患者无汗。
Zotero 插件