Document Detail


Insulin-like growth factor-1 and TNF-alpha regulate autophagy through c-jun N-terminal kinase and Akt pathways in human atherosclerotic vascular smooth cells.
MedLine Citation:
PMID:  16942488     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
A balance between programmed cell death and survival of vascular smooth muscle cells (VSMC) in the fibrous cap, which is primarily composed of VSMC and extracellular matrix, appears to best correlate with plaque instability or stability and is controlled by growth factors and cytokines. Autophagy is also involved in programmed cell death. We assessed the effect of TNF-alpha and insulin-like growth factor-1 (IGF-1) on the expression of autophagic genes, microtubule-associated protein 1 light chain 3 (MAPLC-3) and Beclin-1 in VSMC isolated from atherosclerotic plaques. Transmission electron microscopy showed a significantly higher number of vacuolated cells in the TNF-alpha-treated VSMC and a markedly lower number in the IGF-1-treated VSMC when compared with the untreated control group. TNF-alpha-induced MAPLC-3 mRNA expression through c-jun N-terminal kinase and protein kinase B pathways and induced Beclin-1 protein expression through the c-jun N-terminal kinase pathway. Expression of MAPLC-3 and Beclin-1 correlated with autophagic cell death of plaque VSMC. IGF-1 inhibited MAPLC-3 mRNA transcripts through the Akt pathway. These findings suggest that the expression of autophagy genes can be influenced by IGF-1 and TNF-alpha through c-jun N-terminal kinase or Akt pathways and autophagy might be involved in the regulation of plaque stability.
Authors:
Guanghong Jia; Gang Cheng; Deepak M Gangahar; Devendra K Agrawal
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural    
Journal Detail:
Title:  Immunology and cell biology     Volume:  84     ISSN:  0818-9641     ISO Abbreviation:  Immunol. Cell Biol.     Publication Date:  2006 Oct 
Date Detail:
Created Date:  2006-08-31     Completed Date:  2006-11-07     Revised Date:  2009-11-19    
Medline Journal Info:
Nlm Unique ID:  8706300     Medline TA:  Immunol Cell Biol     Country:  Australia    
Other Details:
Languages:  eng     Pagination:  448-54     Citation Subset:  IM    
Affiliation:
Department of Biomedical Sciences, Creighton University School of Medicine, Omaha, Nebraska 68178, USA.
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MeSH Terms
Descriptor/Qualifier:
Apoptosis Regulatory Proteins / genetics,  metabolism
Atherosclerosis / metabolism*,  pathology
Autophagy*
Blotting, Western
Carotid Stenosis / immunology,  metabolism,  surgery
Cell Separation
Humans
Insulin-Like Growth Factor I / pharmacology,  physiology*
JNK Mitogen-Activated Protein Kinases / metabolism
Membrane Proteins / genetics,  metabolism
Microscopy, Electron, Transmission
Microtubule-Associated Proteins / genetics,  metabolism
Muscle, Smooth, Vascular / cytology*
Myocytes, Smooth Muscle / metabolism,  physiology*
Proto-Oncogene Proteins c-akt / metabolism
Reverse Transcriptase Polymerase Chain Reaction
Signal Transduction*
Tumor Necrosis Factor-alpha / pharmacology,  physiology*
Grant Support
ID/Acronym/Agency:
R01HL070885/HL/NHLBI NIH HHS; R01HL073349/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/Apoptosis Regulatory Proteins; 0/BECN1 protein, human; 0/Membrane Proteins; 0/Microtubule-Associated Proteins; 0/Tumor Necrosis Factor-alpha; 0/light chain 3, human; 67763-96-6/Insulin-Like Growth Factor I; EC 2.7.11.1/Proto-Oncogene Proteins c-akt; EC 2.7.11.24/JNK Mitogen-Activated Protein Kinases
Comments/Corrections
Comment In:
Autophagy. 2007 Jan-Feb;3(1):63-4   [PMID:  17172800 ]

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


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