Journal
JOURNAL OF PHARMACOLOGICAL SCIENCES
Volume 116, Issue 1, Pages 1-5Publisher
JAPANESE PHARMACOLOGICAL SOC
DOI: 10.1254/jphs.11R01CP
Keywords
hydrogen sulfide; gasotransmitter; pancreatic beta-cell; cytoprotection; diabetes mellitus
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Funding
- Japan Society Promotion of Science [21591146, 22790255]
- Oita University
- Venture Business Laboratory, Oita University
- Oita Broadcasting System Cultural Foundation
- Grants-in-Aid for Scientific Research [22790255, 21591146] Funding Source: KAKEN
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Hydrogen sulfide (H2S) is an important signaling molecule in various mammalian cells and tissues. H2S is synthesized from L-cysteine and regulates several cellular and physiological phenomena (vasorelaxation, hormone secretion, and apoptosis) and multicellular events (neuromodulation and inflammatory responses). H2S can be produced in pancreatic beta-cells by cystathionine beta-synthase (CBS) or cystathionine gamma-lyase (CSE). H(2)5 inhibits insulin release and regulates beta-cell survival. We found that glucose stimulation increased CSE expression at transcript and protein levels in mouse pancreatic islets. We also found that H2S protects beta-cells that were chronically exposed to high glucose from apoptotic cell death. Loss of beta-cell mass and failures of beta-cell function are important in the pathogenesis and/or progression of diabetes mellitus; therefore, molecular analyses of the mechanisms of H2S production and its protective effects on beta-cells may lead to new insights into diabetes mellitus.
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