S-Space College of Medicine/School of Medicine (의과대학/대학원) Molecular and Genomic Medicine (분자유전체의학전공) Journal Papers (저널논문_분자유전체의학전공)
Involvement of Ca2+-mediated apoptotic signals in palmitate-induced MIN6N8a beta cell death
- Choi, Sung-E; Kim, Hyo-Eun; Shin, Ha-Chul; Jang, Hyun-Ju; Lee, Kwan-Woo; Kim, Youngsoo; Kang, Sang Sun; Chun, Jaesun; Kang, Yup
- Issue Date
- Mol Cell Endocrinol. 2007 Jun 30;272(1-2):50-62. Epub 2007 Apr 22.
- Animals; Apoptosis/*drug effects; Calcineurin/physiology; Calcium/antagonists & inhibitors/*physiology; Cell Death/drug effects; Cell Line; Chelating Agents/pharmacology; Endoplasmic Reticulum/drug effects; Insulin-Secreting Cells/*drug effects/physiology; Male; Mice; Oncogene Protein v-akt/metabolism; Palmitic Acid/*pharmacology; Protective Agents/pharmacology; Rats; Rats, Sprague-Dawley; Signal Transduction/drug effects; bcl-Associated Death Protein/metabolism
- 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.
- 0303-7207 (Print)
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