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Involvement of Ca2+-mediated apoptotic signals in palmitate-induced MIN6N8a beta cell death
Cited 41 time in
Web of Science
Cited 43 time in Scopus
- Authors
- Issue Date
- 2007-05-18
- Publisher
- Elsevier
- Citation
- Mol Cell Endocrinol. 2007 Jun 30;272(1-2):50-62. Epub 2007 Apr 22.
- Keywords
- 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
- 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.
- ISSN
- 0303-7207 (Print)
- Language
- English
- URI
- http://www.sciencedirect.com/science?_ob=ArticleURL&_udi=B6T3G-4NJG43R-1&_user=10&_rdoc=1&_fmt=&_orig=search&_sort=d&_docanchor=&view=c&_acct=C000050221&_version=1&_urlVersion=0&_userid=10&md5=3f24636290dffb9e5750e5126026229a
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=17507155
https://hdl.handle.net/10371/26551
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