Document Detail

Connexins protect mouse pancreatic β cells against apoptosis.
MedLine Citation:
PMID:  22056383     Owner:  NLM     Status:  MEDLINE    
Type 1 diabetes develops when most insulin-producing β cells of the pancreas are killed by an autoimmune attack. The in vivo conditions modulating the sensitivity and resistance of β cells to this attack remain largely obscure. Here, we show that connexin 36 (Cx36), a trans-membrane protein that forms gap junctions between β cells in the pancreatic islets, protects mouse β cells against both cytotoxic drugs and cytokines that prevail in the islet environment at the onset of type 1 diabetes. We documented that this protection was at least partially dependent on intercellular communication, which Cx36 and other types of connexin channels establish within pancreatic islets. We further found that proinflammatory cytokines decreased expression of Cx36 and that experimental reduction or augmentation of Cx36 levels increased or decreased β cell apoptosis, respectively. Thus, we conclude that Cx36 is central to β cell protection from toxic insults.
Philippe Klee; Florent Allagnat; Helena Pontes; Manon Cederroth; Anne Charollais; Dorothée Caille; Aurore Britan; Jacques-Antoine Haefliger; Paolo Meda
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2011-11-07
Journal Detail:
Title:  The Journal of clinical investigation     Volume:  121     ISSN:  1558-8238     ISO Abbreviation:  J. Clin. Invest.     Publication Date:  2011 Dec 
Date Detail:
Created Date:  2011-12-02     Completed Date:  2012-01-31     Revised Date:  2013-06-27    
Medline Journal Info:
Nlm Unique ID:  7802877     Medline TA:  J Clin Invest     Country:  United States    
Other Details:
Languages:  eng     Pagination:  4870-9     Citation Subset:  AIM; IM    
Department of Cell Physiology and Metabolism, University of Geneva, Medical School, Geneva, Switzerland.
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MeSH Terms
Alloxan / pharmacology,  toxicity
Apoptosis / drug effects
Cell Communication
Cellular Microenvironment
Connexins / antagonists & inhibitors,  deficiency,  genetics,  physiology*
Diabetes Mellitus, Experimental / chemically induced,  metabolism,  pathology,  prevention & control*
Gap Junctions / physiology
Gene Dosage
Insulin / genetics
Interferon-gamma / toxicity
Interleukin-1beta / toxicity
Islets of Langerhans / drug effects,  metabolism,  pathology*
Mice, Inbred C57BL
Mice, Knockout
Mice, Transgenic
Nitric Oxide / biosynthesis
Promoter Regions, Genetic
RNA Interference
RNA, Small Interfering / pharmacology
Recombinant Fusion Proteins / physiology
Streptozocin / pharmacology,  toxicity
Tumor Necrosis Factor-alpha / toxicity
Reg. No./Substance:
0/Connexins; 0/Insulin; 0/Interleukin-1beta; 0/RNA, Small Interfering; 0/Recombinant Fusion Proteins; 0/Tumor Necrosis Factor-alpha; 0/connexin 36; 10102-43-9/Nitric Oxide; 18883-66-4/Streptozocin; 50-71-5/Alloxan; 82115-62-6/Interferon-gamma

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

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