Format

Send to

Choose Destination
Cell Calcium. 2017 May;63:53-59. doi: 10.1016/j.ceca.2016.12.004. Epub 2016 Dec 21.

Regulation of epithelial ion transport in exocrine glands by store-operated Ca2+ entry.

Author information

1
Department of Pathology, New York University School of Medicine, New York, NY, 10016, USA.
2
Department of Pathology, New York University School of Medicine, New York, NY, 10016, USA. Electronic address: feskes01@nyumc.org.

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.

KEYWORDS:

CaCC; Fluid secretion; ORAI1; STIM1; Sweat glands; TMEM16A

PMID:
28027799
PMCID:
PMC5466487
DOI:
10.1016/j.ceca.2016.12.004
[Indexed for MEDLINE]
Free PMC Article

Supplemental Content

Full text links

Icon for Elsevier Science Icon for PubMed Central
Loading ...
Support Center