title: Regulation of epithelial ion transport in exocrine glands by store-operated Ca2+entry.
abstract: Store-operated Ca2+entry (SOCE) is a conserved mechanism of Ca2+influx that regulates Ca2+signaling in many cell types. SOCE is activated by depletion of endoplasmic reticulum (ER) Ca2+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 Ca2+-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 Ca2+-activated chloride channel TMEM16A is inactive and fails to secrete Cl-, resulting in anhidrosis in mice and human patients.
authors.affiliation: Department of Pathology, New York University School of Medicine, New York, NY, 10016, USA.
authors.forename: Axel R
authors.initials: AR
authors.lastname: Concepcion
authors.affiliation: Department of Pathology, New York University School of Medicine, New York, NY, 10016, USA. Electronic address: feskes01@nyumc.org.
authors.forename: Stefan
authors.initials: S
authors.lastname: Feske
mesh_terms: D000818:Animals; D002118:Calcium / Q000378:metabolism*; D015220:Calcium Channels / Q000378:metabolism*; D020013:Calcium Signaling / Q000502:physiology*; D004847:Epithelial Cells / Q000378:metabolism*; D005088:Exocrine Glands / Q000378:metabolism*; D006801:Humans; D017136:Ion Transport
chemical_list: D015220:Calcium Channels; D002118:Calcium
keywords: CaCC; Fluid secretion; ORAI1; STIM1; Sweat glands; TMEM16A