| VIP down-regulates the inflammatory potential and promotes survival of dying (neural crest-derived) corneal endothelial cells ex vivo: necrosis to apoptosis switch and up-regulation of Bcl-2 and N-cadherin. | |
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MedLine Citation:
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PMID: 19250342 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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The neuropeptide vasoactive intestinal peptide (VIP) is anti-inflammatory and protective in the immune and nervous systems, respectively. This study demonstrated in corneal endothelial (CE) cells injured by severe oxidative stress (1.4 mM H(2)O(2)) in bovine corneal organ cultures that VIP pre-treatment (0, 10(-10), 10(-8), and 10(-6) M; 15 min), in a VIP concentration-dependent manner, switched the inflammation-causing necrosis to inflammation-neutral apoptosis (showing annexin V-binding, chromatin condensation, and DNA fragmentation) and upheld ATP levels in a VIP antagonist (SN)VIPhyb-sensitive manner, while up-regulated mRNA levels of the anti-apoptotic Bcl-2 and the differentiation marker N-cadherin in a kinase A inhibitor-sensitive manner. As a result, VIP, in a concentration-dependent and VIP antagonist-sensitive manners, promoted long-term CE cell survival. ATP levels, a determining factor in the choice of apoptosis versus necrosis, measured after VIP pre-treatment and 0.5 min post-H(2)O(2) were 39.6 +/- 3.3, 50.8 +/- 6.2, 60.1 +/- 4.8, and 53.6 +/- 5.3 pmoles/microg protein (mean +/- SEM), respectively (p < 0.05, anova). VIP treatment alone concentration-dependently increased levels of N-cadherin (Koh et al. 2008), the phosphorylated cAMP-responsive-element binding protein and Bcl-2, while 10(-8) M VIP, in a VIP antagonist (SN)VIPhyb-sensitive manner, increased ATP level by 38% (p < 0.02) and decreased glycogen level by 32% (p < 0.02). VPAC1 (not VPAC2) receptor was expressed in CE cells. Thus, CE cell VIP/VPAC1 signaling is both anti-inflammatory and protective in the corneal endothelium. |
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Authors:
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Shay-Whey M Koh; Jason Cheng; Rebecca M Dodson; Chao-Yar T Ku; Cara J Abbondandolo |
Publication Detail:
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Type: In Vitro; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't Date: 2009-02-24 |
Journal Detail:
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Title: Journal of neurochemistry Volume: 109 ISSN: 1471-4159 ISO Abbreviation: J. Neurochem. Publication Date: 2009 May |
Date Detail:
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Created Date: 2009-05-05 Completed Date: 2009-06-09 Revised Date: 2011-10-21 |
Medline Journal Info:
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Nlm Unique ID: 2985190R Medline TA: J Neurochem Country: England |
Other Details:
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Languages: eng Pagination: 792-806 Citation Subset: IM |
Affiliation:
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Department of Ophthalmology & Visual Sciences, University of Maryland, Baltimore, Maryland 21201, USA. skoh@umaryland.edu |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Adenosine Triphosphate
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metabolism Animals Annexin A5 / metabolism Apoptosis / drug effects Cadherins / genetics, metabolism* Cattle Cell Survival / drug effects Dose-Response Relationship, Drug Endothelial Cells / drug effects* Epithelium, Corneal / cytology* Gene Expression Regulation / drug effects* Glycogen / metabolism Hydrogen Peroxide / toxicity Necrosis / chemically induced, prevention & control* Oxidants / toxicity Oxidative Stress / drug effects, physiology Propidium / diagnostic use Proto-Oncogene Proteins / genetics, metabolism* RNA, Messenger / metabolism Vasoactive Intestinal Peptide / pharmacology* |
| Grant Support | |
ID/Acronym/Agency:
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R01 EY011607-08/EY/NEI NIH HHS; R01EY-11607/EY/NEI NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Annexin A5; 0/Cadherins; 0/Oxidants; 0/Proto-Oncogene Proteins; 0/RNA, Messenger; 36015-30-2/Propidium; 37221-79-7/Vasoactive Intestinal Peptide; 56-65-5/Adenosine Triphosphate; 7722-84-1/Hydrogen Peroxide; 9005-79-2/Glycogen |
| Comments/Corrections | |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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