| Regulation of podocyte survival and endoplasmic reticulum stress by fatty acids. | |
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MedLine Citation:
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PMID: 20668104 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Apoptosis of podocytes is considered critical in the pathogenesis of diabetic nephropathy (DN). Free fatty acids (FFAs) are critically involved in the pathogenesis of diabetes mellitus type 2, in particular the regulation of pancreatic β cell survival. The objectives of this study were to elucidate the role of palmitic acid, palmitoleic, and oleic acid in the regulation of podocyte cell death and endoplasmic reticulum (ER) stress. We show that palmitic acid increases podocyte cell death, both apoptosis and necrosis of podocytes, in a dose and time-dependent fashion. Palmitic acid induces podocyte ER stress, leading to an unfolded protein response as reflected by the induction of the ER chaperone immunoglobulin heavy chain binding protein (BiP) and proapoptotic C/EBP homologous protein (CHOP) transcription factor. Of note, the monounsaturated palmitoleic and oleic acid can attenuate the palmitic acid-induced upregulation of CHOP, thereby preventing cell death. Similarly, gene silencing of CHOP protects against palmitic acid-induced podocyte apoptosis. Our results offer a rationale for interventional studies aimed at testing whether dietary shifting of the FFA balance toward unsaturated FFAs can delay the progression of DN. |
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Authors:
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Jonas Sieber; Maja Tamara Lindenmeyer; Kapil Kampe; Kirk Nicholas Campbell; Clemens David Cohen; Helmut Hopfer; Peter Mundel; Andreas Werner Jehle |
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Publication Detail:
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Type: Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't Date: 2010-07-28 |
Journal Detail:
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Title: American journal of physiology. Renal physiology Volume: 299 ISSN: 1522-1466 ISO Abbreviation: Am. J. Physiol. Renal Physiol. Publication Date: 2010 Oct |
Date Detail:
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Created Date: 2010-10-04 Completed Date: 2010-10-26 Revised Date: 2012-05-07 |
Medline Journal Info:
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Nlm Unique ID: 100901990 Medline TA: Am J Physiol Renal Physiol Country: United States |
Other Details:
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Languages: eng Pagination: F821-9 Citation Subset: IM |
Affiliation:
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Dept. of Biomedicine, Molecular Nephrology, Univ. Hospital Basel, Hebelstrasse 20, 4031 Basel, Switzerland. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Animals Apoptosis / drug effects* Caspase 3 / metabolism Cell Survival / drug effects Cells, Cultured Endoplasmic Reticulum / drug effects*, physiology Fatty Acids, Monounsaturated / pharmacology* Gene Silencing Mice Models, Animal Oleic Acid / pharmacology* Palmitic Acid / pharmacology* Podocytes / cytology, drug effects*, metabolism Stress, Physiological / physiology* Transcription Factor CHOP / genetics, metabolism |
| Grant Support | |
ID/Acronym/Agency:
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DK57683/DK/NIDDK NIH HHS; DK62472/DK/NIDDK NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Ddit3 protein, mouse; 0/Fatty Acids, Monounsaturated; 112-80-1/Oleic Acid; 147336-12-7/Transcription Factor CHOP; 2091-29-4/palmitoleic acid; 57-10-3/Palmitic Acid; EC 3.4.22.-/Caspase 3 |
| Comments/Corrections | |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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