期刊
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
卷 101, 期 27, 页码 10090-10094出版社
NATL ACAD SCIENCES
DOI: 10.1073/pnas.0403551101
关键词
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资金
- NIDDK NIH HHS [R01 DK058508, DK58508] Funding Source: Medline
In type 1 diabetes (T1D), there is a specific destruction of the insulin secreting pancreatic beta cell. Although the exact molecular mechanisms underlying beta cell destruction are not known, sera from T1D patients have been shown to promote Ca2+-induced apoptosis. We now demonstrate that apolipoprotein CIII (apoCIII) is increased in serum from T1D patients and that this serum factor both induces increased cytoplasmic free intracellular Ca2+ concentration ([Ca2+](i)) and beta cell death. The apoCIII-induced increase in [Ca2+](i) reflects an activation of the voltage-gated L-type Ca2+ channel. Both the effects of T1D sera and apoCIII on the beta cell are abolished in the presence of antibody against apoCIII. Increased serum levels of apoCIII can thus account for the increase in beta cell [Ca2+](i) and thereby beta cell apoptosis associated with T1D.
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