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dc.contributor.authorLi, Jian-ming
dc.contributor.authorZhang, Xueqing
dc.contributor.authorNelson, Peter R.
dc.contributor.authorOdgren, Paul R.
dc.contributor.authorNelson, Janice D.
dc.contributor.authorVasiliu, Calin A.
dc.contributor.authorPark, Jane
dc.contributor.authorMorris, Marvin
dc.contributor.authorLian, Jane B.
dc.contributor.authorCutler, Bruce S.
dc.contributor.authorNewburger, Peter E.
dc.date2022-08-11T08:10:07.000
dc.date.accessioned2022-08-23T16:56:13Z
dc.date.available2022-08-23T16:56:13Z
dc.date.issued2007-05-15
dc.date.submitted2011-02-16
dc.identifier.citationJ Cell Biochem. 2007 May 15;101(2):399-410. <a href="http://dx.doi.org/10.1002/jcb.21190">Link to article on publisher's site</a>
dc.identifier.issn0730-2312 (Linking)
dc.identifier.doi10.1002/jcb.21190
dc.identifier.pmid17171642
dc.identifier.urihttp://hdl.handle.net/20.500.14038/42878
dc.description.abstractThe success of vascular intervention including angioplasty, stenting, and arterial bypass remains limited by negative remodeling resulted in lumen restenosis. This study was to characterize the global transcription profile reflecting concurrent events along arterial remodeling and neointima formation in a rat carotid artery balloon-injury model. Expression profiling of injured and control common carotid arteries on days 4, 7, 14 post-injury that mark the major pathohistological progression stages of neointimal formation were recorded on high-density oligonucleotide arrays. A subset of genes from microarray-based data was further studied using quantitative real time RT-PCR and in situ hybridization with sequential arterial samples from days 1 to 28 post-injury. The gene-encoded proteins were validated with Western blot. Besides temporal induction of a large cluster of genes over-represented by cell proliferation and macromolecule metabolism gene ontology categories, a fast-evolving inflammation could be demonstrated by the induction of Tgfb and other anti-inflammatory genes (e.g., C1qtnf3 (C1q and tumor necrosis factor related protein 3 (predicted))) and a shift from type 1 to 2 helper T cell response. The most significant signature of the induced neointimal profile is enrichment of genes functionally related to angiogenesis and extracellular matrix (ECM) remodeling (e.g., Spp1 (secreted phosphoprotein 1), CD44 (CD44 antigen), and Cxcl12 (chemokine (C-X-C motif) ligand 12 (stromal cell-derived factor 1)). Some of the genes represent stress-responsive mesenchymal stromal cell cytokines. This study highlighted mesenchymal stromal cell cytokines-driven inflammatory extracellular matrix remodeling, as target processes for potential clinical therapeutic intervention.
dc.language.isoen_US
dc.relation<a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&list_uids=17171642&dopt=Abstract">Link to Article in PubMed</a>
dc.relation.urlhttp://dx.doi.org/10.1002/jcb.21190
dc.subject*Angioplasty, Balloon
dc.subjectAnimals
dc.subject*Carotid Arteries
dc.subjectComputational Biology
dc.subjectGene Expression Profiling
dc.subject*Gene Expression Regulation
dc.subjectHyperplasia
dc.subjectIn Situ Hybridization
dc.subjectIntercellular Signaling Peptides and Proteins
dc.subjectMale
dc.subjectOligonucleotide Array Sequence Analysis
dc.subjectOxidative Stress
dc.subjectRats
dc.subjectRats, Sprague-Dawley
dc.subjectCell Biology
dc.titleTemporal evolution of gene expression in rat carotid artery following balloon angioplasty
dc.typeJournal Article
dc.source.journaltitleJournal of cellular biochemistry
dc.source.volume101
dc.source.issue2
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/odgren/7
dc.identifier.contextkey1789902
html.description.abstract<p>The success of vascular intervention including angioplasty, stenting, and arterial bypass remains limited by negative remodeling resulted in lumen restenosis. This study was to characterize the global transcription profile reflecting concurrent events along arterial remodeling and neointima formation in a rat carotid artery balloon-injury model. Expression profiling of injured and control common carotid arteries on days 4, 7, 14 post-injury that mark the major pathohistological progression stages of neointimal formation were recorded on high-density oligonucleotide arrays. A subset of genes from microarray-based data was further studied using quantitative real time RT-PCR and in situ hybridization with sequential arterial samples from days 1 to 28 post-injury. The gene-encoded proteins were validated with Western blot. Besides temporal induction of a large cluster of genes over-represented by cell proliferation and macromolecule metabolism gene ontology categories, a fast-evolving inflammation could be demonstrated by the induction of Tgfb and other anti-inflammatory genes (e.g., C1qtnf3 (C1q and tumor necrosis factor related protein 3 (predicted))) and a shift from type 1 to 2 helper T cell response. The most significant signature of the induced neointimal profile is enrichment of genes functionally related to angiogenesis and extracellular matrix (ECM) remodeling (e.g., Spp1 (secreted phosphoprotein 1), CD44 (CD44 antigen), and Cxcl12 (chemokine (C-X-C motif) ligand 12 (stromal cell-derived factor 1)). Some of the genes represent stress-responsive mesenchymal stromal cell cytokines. This study highlighted mesenchymal stromal cell cytokines-driven inflammatory extracellular matrix remodeling, as target processes for potential clinical therapeutic intervention.</p>
dc.identifier.submissionpathodgren/7
dc.contributor.departmentDepartment of Pediatrics
dc.contributor.departmentDepartment of Cell Biology
dc.contributor.departmentDepartment of Surgery
dc.source.pages399-410


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