ArticleJournal of molecular medicine (Berlin, Germany)2006
Fibroblast migration after myocardial infarction is regulated by transient SPARC expression.
Article in Journal of molecular medicine (Berlin, Germany), 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 37 citations in OpenAlex.
- Article
- Article
- Cyanidin prevents cardiomyocyte apoptosis in mice after myocardial infarction.Naunyn-Schmiedeberg's archives of pharmacology · 2024Article
- Sex-related differences of early cardiac functional and proteomic alterations in a rat model of myocardial ischemia.Journal of translational medicine · 2021Article
- Myocardial infarction remodeling that progresses to heart failure: a signaling misunderstanding.American journal of physiology. Heart and circulatory physiology · 2018Review
- Angiokine Wisp-1 is increased in myocardial infarction and regulates cardiac endothelial signaling.JCI insight · 2018Article
- Extracellular Matrix and Dermal Fibroblast Function in the Healing Wound.Advances in wound care · 2016Review
- Predictive value of circulating osteonectin in patients with ischemic symptomatic chronic heart failure.Biomedical journal · 2015Observational
- Integrins protect cardiomyocytes from ischemia/reperfusion injury.The Journal of clinical investigation · 2013Article
- Matricellular proteins in cardiac adaptation and disease.Physiological reviews · 2012Review
- Quantitative N-linked glycoproteomics of myocardial ischemia and reperfusion injury reveals early remodeling in the extracellular environment.Molecular & cellular proteomics : MCP · 2011Article
- SPARC downregulation attenuates the profibrogenic response of hepatic stellate cells induced by TGF-β1 and PDGF.American journal of physiology. Gastrointestinal and liver physiology · 2011Article
- Transcriptome analysis of the desert locust central nervous system: production and annotation of a Schistocerca gregaria EST database.PloS one · 2011Article
- SPARC/osteonectin functions to maintain homeostasis of the collagenous extracellular matrix in the periodontal ligament.The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society · 2010Article
- Extracellular matrix roles during cardiac repair.Life sciences · 2010Review
- SPARC: a key player in the pathologies associated with obesity and diabetes.Nature reviews. Endocrinology · 2010Review
- Cardiac extracellular matrix remodeling: fibrillar collagens and Secreted Protein Acidic and Rich in Cysteine (SPARC).Journal of molecular and cellular cardiology · 2010Review
- Role of healing-specific-matricellular proteins and matrix metalloproteinases in age-related enhanced early remodeling after reperfused STEMI in dogs.Molecular and cellular biochemistry · 2009Article
- IFATS collection: Combinatorial peptides identify alpha5beta1 integrin as a receptor for the matricellular protein SPARC on adipose stromal cells.Stem cells (Dayton, Ohio) · 2008Article
- CEACAMs: their role in physiology and pathophysiology.Current opinion in cell biology · 2006Review
Corrections and comments
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Secreted protein, acidic, and rich in cysteine (SPARC) is thought to regulate cell matrix interaction during wound repair. We hypothesized that SPARC might promote migration via integrin-dependent mechanisms. The present study was designed to clarify the contribution of SPARC in the wound healing process after myocardial infarction (MI). Adult mice received a specific alpha(v) integrin inhibitor or vehicle through osmotic mini pumps. Mice of each group were either sham-operated or MI was induced. SPARC expression was investigated 2 days, 7 days, and 1 month after the surgical procedure. For migration assays, a modified Boyden chamber assay was used. A transient increase of SPARC levels was observed, starting at day 2 (2.55+/-0.21), day 7 (3.72+/-0.28), and 1 month (1.9+/-0.16) after MI. After 2 months, SPARC expression dropped back to normal levels compared to sham-operated hearts. Immunofluorescence analysis showed an increase of SPARC in the infarcted area 2 days after MI, a strong increase in the scar area 7 days after MI, and only low levels in the scar area 2 months after MI. Integrin alpha(v) inhibition abolished the up-regulation of SPARC. In vitro migration assays demonstrated that fibronectin-stimulated haptotaxis of fibroblasts was modulated by SPARC. This study provides evidence that SPARC is significantly up-regulated in the infarcted region after MI. This up-regulation is dependent on alpha(v) integrins. As SPARC is found to regulate fibroblast migration, it appears to play an important role in the injured myocardium with regard to healing and scar formation.
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