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

Choi, SE; Kim, HE; Shin, HC; Jang, HJ; Lee, KW; Kim, Y; Kang, SS; Chun, J; Kangv, Y
Molecular and cellular endocrinology, 272(1-2):50-62, 2007
Journal Title
Molecular and cellular endocrinology
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.
MeSH terms
AnimalsApoptosis/drug effects*Calcineurin/physiologyCalcium/antagonists & inhibitorsCalcium/physiology*Cell Death/drug effectsCell LineChelating Agents/pharmacologyEndoplasmic Reticulum/drug effectsInsulin-Secreting Cells/drug effects*Insulin-Secreting Cells/physiologyMaleMiceOncogene Protein v-akt/metabolismPalmitic Acid/pharmacology*Protective Agents/pharmacologyRatsRats, Sprague-DawleySignal Transduction/drug effectsbcl-Associated Death Protein/metabolism
Appears in Collections:
Journal Papers > Research Organization > Chronic Inflammatory Disease Research Center
Journal Papers > School of Medicine / Graduate School of Medicine > Endocrinology & Metabolism
Journal Papers > School of Medicine / Graduate School of Medicine > Physiology
AJOU Authors
최, 성이이, 관우강, 엽
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