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Mol Cell Endocrinol. 2007 Jun 30;272(1-2):50-62. Epub 2007 Apr 22.

Involvement of Ca2+-mediated apoptotic signals in palmitate-induced MIN6N8a beta cell death.

Author information

1
Institute for Medical Science, Ajou University School of Medicine, 442-749 Suwon, Republic of Korea.

Abstract

The extracellular Ca(2+) chelator EGTA and L-type Ca(2+) channel blockers, such as, nifedipine and nimodipine were found to have a protective effect on palmitate-induced MIN6N8a beta cell apoptosis, whereas the Ca(2+) channel opener, Bay K8644, enhanced the apoptotic process. Moreover, the phospho-form of Bad, in conjunction with phospho-Akt, was reduced in response to palmitate and the palmitate-induced dephosphorylations of Akt and Bad were dependent on Ca(2+) influx. The transient expression of catalytically active Akt prevented MIN6N8a cells from palmitate-induced apoptosis. Deltamethrin, an inhibitor of Ca(2+)-activated phosphatase, delayed Akt and Bad dephosphorylations, and then protected MIN6N8a cells from palmitate-induced apoptosis. On the other hand, palmitate was found to induce CHOP, an apoptotic transcription factor in response to ER stress, and this induction was enhanced by Ca(2+) influx. Our studies suggested that Ca(2+) influx and subsequent Ca(2+)-mediated apoptotic signals are involved in palmitate-induced beta cell death.

PMID:
17507155
DOI:
10.1016/j.mce.2007.04.004
[Indexed for MEDLINE]

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