| Anti-inflammatory cytokine interleukin-19 inhibits smooth muscle cell migration and activation of cytoskeletal regulators of VSMC motility. | |
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MedLine Citation:
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PMID: 21209363 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Vascular smooth muscle cell (VSMC) migration is an important cellular event in multiple vascular diseases, including atherosclerosis, restenosis, and transplant vasculopathy. Little is known regarding the effects of anti-inflammatory interleukins on VSMC migration. This study tested the hypothesis that an anti-inflammatory Th2 interleukin, interleukin-19 (IL-19), could decrease VSMC motility. IL-19 significantly decreased platelet-derived growth factor (PDGF)-stimulated VSMC chemotaxis in Boyden chambers and migration in scratch wound assays. IL-19 significantly decreased VSMC spreading in response to PDGF. To determine the molecular mechanism(s) for these cellular effects, we examined the effect of IL-19 on activation of proteins that regulate VSMC cytoskeletal dynamics and locomotion. IL-19 decreased PDGF-driven activation of several cytoskeletal regulatory proteins that play an important role in smooth muscle cell motility, including heat shock protein-27 (HSP27), myosin light chain (MLC), and cofilin. IL-19 decreased PDGF activation of the Rac1 and RhoA GTPases, important integrators of migratory signals. IL-19 was unable to inhibit VSMC migration nor was able to inhibit activation of cytoskeletal regulatory proteins in VSMC transduced with a constitutively active Rac1 mutant (RacV14), suggesting that IL-19 inhibits events proximal to Rac1 activation. Together, these data are the first to indicate that IL-19 can have important inhibitory effects on VSMC motility and activation of cytoskeletal regulatory proteins. This has important implications for the use of anti-inflammatory cytokines in the treatment of vascular occlusive disease. |
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Authors:
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Khatuna Gabunia; Surbhi Jain; Ross N England; Michael V Autieri |
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Publication Detail:
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Type: Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S. Date: 2011-01-05 |
Journal Detail:
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Title: American journal of physiology. Cell physiology Volume: 300 ISSN: 1522-1563 ISO Abbreviation: Am. J. Physiol., Cell Physiol. Publication Date: 2011 Apr |
Date Detail:
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Created Date: 2011-03-29 Completed Date: 2011-05-20 Revised Date: 2012-04-02 |
Medline Journal Info:
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Nlm Unique ID: 100901225 Medline TA: Am J Physiol Cell Physiol Country: United States |
Other Details:
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Languages: eng Pagination: C896-906 Citation Subset: IM |
Affiliation:
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Dept. of Physiology, Independence Blue Cross Cardiovascular Research Center, Temple University School of Medicine, Philadelphia, Pennsylvania 19140, USA. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Adolescent Adult Anti-Inflammatory Agents / pharmacology Cell Movement / drug effects* Cells, Cultured Cytoskeletal Proteins / genetics, metabolism* Cytoskeleton / drug effects*, metabolism HSP27 Heat-Shock Proteins / metabolism Humans Interleukins / pharmacology* Male Myocytes, Smooth Muscle / cytology, drug effects*, physiology* Phosphorylation Platelet-Derived Growth Factor / pharmacology Young Adult rac1 GTP-Binding Protein / metabolism rhoA GTP-Binding Protein / metabolism |
| Grant Support | |
ID/Acronym/Agency:
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HL-090885/HL/NHLBI NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Anti-Inflammatory Agents; 0/Cytoskeletal Proteins; 0/HSP27 Heat-Shock Proteins; 0/IL19 protein, human; 0/Interleukins; 0/Platelet-Derived Growth Factor; EC 3.6.5.2/rac1 GTP-Binding Protein; EC 3.6.5.2/rhoA GTP-Binding Protein |
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