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Priming of insulin granules for exocytosis by granular Cl(-) uptake and acidification
Department of Physiological Sciences, Lund University, Lund.
University of Chicago, Department of Neurobiology, Pharmacology and Physiology, Chicago.
Department of Physiological Sciences, Lund University, Lund.
University of Chicago, Department of Neurobiology, Pharmacology and Physiology, Chicago.
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2001 (English)In: Journal of Cell Science, ISSN 0021-9533, E-ISSN 1477-9137, Vol. 114, no Pt 11, 2145-54 p.Article in journal (Refereed) Published
Abstract [en]

ATP-dependent priming of the secretory granules precedes Ca(2+)-regulated neuroendocrine secretion, but the exact nature of this reaction is not fully established in all secretory cell types. We have further investigated this reaction in the insulin-secreting pancreatic B-cell and demonstrate that granular acidification driven by a V-type H(+)-ATPase in the granular membrane is a decisive step in priming. This requires simultaneous Cl(-) uptake through granular ClC-3 Cl(-) channels. Accordingly, granule acidification and priming are inhibited by agents that prevent transgranular Cl(-) fluxes, such as 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid (DIDS) and an antibody against the ClC-3 channels, but accelerated by increases in the intracellular ATP:ADP ratio or addition of hypoglycemic sulfonylureas. We suggest that this might represent an important mechanism for metabolic regulation of Ca(2+)-dependent exocytosis that is also likely to be operational in other secretory cell types.

Place, publisher, year, edition, pages
2001. Vol. 114, no Pt 11, 2145-54 p.
Keyword [en]
ClC-3 channels, Exocytosis, Granular pH, Insulin, Sulfonylureas
National Category
Medical and Health Sciences Cell Biology
Identifiers
URN: urn:nbn:se:uu:diva-87028PubMedID: 11493650OAI: oai:DiVA.org:uu-87028DiVA: diva2:128151
Available from: 2008-12-12 Created: 2008-12-12 Last updated: 2011-11-19

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PubMedhttp://jcs.biologists.org/cgi/content/full/114/11/2145

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Barg, Sebastian

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