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Tytuł pozycji:

The proapoptotic BH3-only proteins Bim and Puma are downstream of endoplasmic reticulum and mitochondrial oxidative stress in pancreatic islets in response to glucotoxicity.

Tytuł :
The proapoptotic BH3-only proteins Bim and Puma are downstream of endoplasmic reticulum and mitochondrial oxidative stress in pancreatic islets in response to glucotoxicity.
Index Terms :
Sciences bio-médicales et agricoles
Animals
Antioxidants -- pharmacology
Apoptosis -- drug effects
Apoptosis Regulatory Proteins -- deficiency -- genetics -- metabolism
Bcl-2-Like Protein 11
Cell Line
Diabetes Mellitus, Type 2 -- metabolism -- pathology
Endoplasmic Reticulum -- drug effects -- metabolism -- pathology
Endoplasmic Reticulum Stress -- drug effects
Glucose -- metabolism
Humans
Insulin-Secreting Cells -- metabolism -- pathology
Islets of Langerhans -- drug effects -- metabolism -- pathology
Membrane Proteins -- deficiency -- genetics -- metabolism
Mice
Mice, 129 Strain
Mice, Inbred C57BL
Mice, Knockout
Mitochondria -- drug effects -- metabolism -- pathology
Oxidants -- pharmacology
Oxidative Stress -- drug effects
Proto-Oncogene Proteins -- deficiency -- genetics -- metabolism
RNA, Messenger -- metabolism
Ribose -- metabolism
Tissue Culture Techniques
Transcription Factor CHOP -- deficiency -- genetics
Tumor Suppressor Proteins -- deficiency -- genetics -- metabolism
info:eu-repo/semantics/article
info:ulb-repo/semantics/articlePeerReview
info:ulb-repo/semantics/openurl/article
Wydawca :
2014-03
Dodane szczegóły :
Wali, Jibran JA
Rondas, Dieter
McKenzie, M D
Zhao, Y
Elkerbout, L
Fynch, S
Gurzov, Esteban Nicolas
Akira, S
Mathieu, Chantal
Kay, T W H TW
Overbergh, Lut
Strasser, Andreas
Thomas, Helen H.E.
Typ dokumentu :
Zasób elektroniczny
URL :
http://hdl.handle.net/2013/ULB-DIPOT:oai:dipot.ulb.ac.be:2013/260216
http://worldcat.org/search?q=on:EQY+http://difusion-oai.ulb.ac.be/oai/request+DCG_ENTIRE_REPOSITORY+CNTCOLL
Dostępność :
Open access content. Open access content
1 full-text file(s): info:eu-repo/semantics/openAccess
Pozostałe numery :
EQY oai:dipot.ulb.ac.be:2013/260216
uri/info:doi/10.1038/cddis.2014.88
uri/info:pii/cddis201488
uri/info:pmid/24625983
uri/info:pmcid/PMC3973197
https://dipot.ulb.ac.be/dspace/bitstream/2013/260216/4/doi_243843.pdf
1012854688
Źródło wspomagające :
UNIV LIBR DE BRUXELLES
From OAIster®, provided by the OCLC Cooperative.
Numer akcesji :
edsoai.on1012854688
Zasób elektroniczny
Apoptosis of pancreatic beta cells is a feature of type 2 diabetes and its prevention may have therapeutic benefit. High glucose concentrations induce apoptosis of islet cells, and this requires the proapoptotic Bcl-2 homology domain 3 (BH3)-only proteins Bim and Puma. We studied the stress pathways induced by glucotoxicity in beta cells that result in apoptosis. High concentrations of glucose or ribose increased expression of the transcription factor CHOP (C/EBP homologous protein) but not endoplasmic reticulum (ER) chaperones, indicating activation of proapoptotic ER stress signaling. Inhibition of ER stress prevented ribose-induced upregulation of Chop and Puma mRNA, and partially protected islets from glucotoxicity. Loss of Bim or Puma partially protected islets from the canonical ER stressor thapsigargin. The antioxidant N-acetyl-cysteine also partially protected islets from glucotoxicity. Islets deficient in both Bim and Puma, but not Bim or Puma alone, were significantly protected from killing induced by the mitochondrial reactive oxygen species donor rotenone. Our data demonstrate that high concentrations of glucose induce ER and oxidative stress, which causes cell death mediated by Bim and Puma. We observed significantly higher Bim and Puma mRNA in islets of human donors with type 2 diabetes. This indicates that inhibition of Bim and Puma, or their inducers, may prevent beta-cell destruction in type 2 diabetes.
info:eu-repo/semantics/published

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