Stem cell factor induction is associated with mast cell accumulation after canine myocardial ischemia and reperfusion
Myocardial infarction is associated with an intense inflammatory reaction leading to healing and scar formation. Because mast cells are a significant source of fibrogenic factors, we investigated mast cell accumulation and regulation of stem cell factor (SCF), a potent growth and tactic factor for m...
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| Veröffentlicht in: | Circulation (New York, N.Y.) N.Y.), 1998-08, Vol.98 (7), p.687-698 |
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| creator | FRANGOGIANNIS, N. G PERRARD, J. L MENDOZA, L. H BURNS, A. R LINDSEY, M. L BALLANTYNE, C. M MICHAEL, L. H SMITH, C. W ENTMAN, M. L |
| description | Myocardial infarction is associated with an intense inflammatory reaction leading to healing and scar formation. Because mast cells are a significant source of fibrogenic factors, we investigated mast cell accumulation and regulation of stem cell factor (SCF), a potent growth and tactic factor for mast cells, in the healing myocardium.
Using a canine model of myocardial ischemia and reperfusion, we demonstrated a striking increase of mast cell numbers during the healing phase of a myocardial infarction. Mast cell numbers started increasing after 72 hours of reperfusion, showing maximum accumulation in areas of collagen deposition (12.0+/-2.6-fold increase; P |
| doi_str_mv | 10.1161/01.CIR.98.7.687 |
| format | Article |
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Using a canine model of myocardial ischemia and reperfusion, we demonstrated a striking increase of mast cell numbers during the healing phase of a myocardial infarction. Mast cell numbers started increasing after 72 hours of reperfusion, showing maximum accumulation in areas of collagen deposition (12.0+/-2.6-fold increase; P<0.01) and proliferating cell nuclear antigen (PCNA) expression. The majority of proliferating cells were identified as alpha-smooth muscle actin-positive myofibroblasts or factor VIII-positive endothelial cells. Mast cells did not appear to proliferate. Using a nuclease protection assay, we demonstrated induction of SCF mRNA within 72 hours of reperfusion. Immunohistochemical studies demonstrated that a subset of macrophages was the source of SCF immunoreactivity in the infarcted myocardium. SCF protein was not found in endothelial cells and myofibroblasts. Intravascular tryptase-positive, FITC-avidin-positive, CD11b-negative mast cell precursors were noted in the area of healing and in the cardiac lymph after 48 to 72 hours of reperfusion.
Mast cells increase in number in areas of collagen deposition and PCNA expression after myocardial ischemia. The data provide evidence of mast cell precursor infiltration into the areas of cellular injury. SCF is induced in a subset of macrophages infiltrating the healing myocardium. We suggest an important role for SCF in promoting chemotaxis and growth of mast cell precursors in the healing heart.</description><identifier>ISSN: 0009-7322</identifier><identifier>EISSN: 1524-4539</identifier><identifier>DOI: 10.1161/01.CIR.98.7.687</identifier><identifier>PMID: 9715862</identifier><identifier>CODEN: CIRCAZ</identifier><language>eng</language><publisher>Hagerstown, MD: Lippincott Williams & Wilkins</publisher><subject>Animals ; Biological and medical sciences ; Cardiology. Vascular system ; Cell Division ; Cloning, Molecular ; Collagen - biosynthesis ; Coronary heart disease ; Dogs ; Endothelium, Vascular - metabolism ; Endothelium, Vascular - pathology ; Factor VIII - analysis ; Female ; Heart ; Male ; Mast Cells - metabolism ; Mast Cells - pathology ; Medical sciences ; Myocardial Infarction - metabolism ; Myocardial Infarction - pathology ; Myocardial Ischemia - metabolism ; Myocardial Ischemia - pathology ; Myocardial Reperfusion ; Polymerase Chain Reaction ; Proliferating Cell Nuclear Antigen - analysis ; Proliferating Cell Nuclear Antigen - biosynthesis ; Recombinant Proteins - biosynthesis ; Stem Cell Factor - biosynthesis ; Time Factors</subject><ispartof>Circulation (New York, N.Y.), 1998-08, Vol.98 (7), p.687-698</ispartof><rights>1998 INIST-CNRS</rights><rights>Copyright American Heart Association, Inc. Aug 18, 1998</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c475t-345153d76b78d230f8ee3b44ec7ed53975e6928b16398ee58ca8fe508d32d6293</citedby><cites>FETCH-LOGICAL-c475t-345153d76b78d230f8ee3b44ec7ed53975e6928b16398ee58ca8fe508d32d6293</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,3673,27903,27904</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=2367818$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/9715862$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>FRANGOGIANNIS, N. G</creatorcontrib><creatorcontrib>PERRARD, J. L</creatorcontrib><creatorcontrib>MENDOZA, L. H</creatorcontrib><creatorcontrib>BURNS, A. R</creatorcontrib><creatorcontrib>LINDSEY, M. L</creatorcontrib><creatorcontrib>BALLANTYNE, C. M</creatorcontrib><creatorcontrib>MICHAEL, L. H</creatorcontrib><creatorcontrib>SMITH, C. W</creatorcontrib><creatorcontrib>ENTMAN, M. L</creatorcontrib><title>Stem cell factor induction is associated with mast cell accumulation after canine myocardial ischemia and reperfusion</title><title>Circulation (New York, N.Y.)</title><addtitle>Circulation</addtitle><description>Myocardial infarction is associated with an intense inflammatory reaction leading to healing and scar formation. Because mast cells are a significant source of fibrogenic factors, we investigated mast cell accumulation and regulation of stem cell factor (SCF), a potent growth and tactic factor for mast cells, in the healing myocardium.
Using a canine model of myocardial ischemia and reperfusion, we demonstrated a striking increase of mast cell numbers during the healing phase of a myocardial infarction. Mast cell numbers started increasing after 72 hours of reperfusion, showing maximum accumulation in areas of collagen deposition (12.0+/-2.6-fold increase; P<0.01) and proliferating cell nuclear antigen (PCNA) expression. The majority of proliferating cells were identified as alpha-smooth muscle actin-positive myofibroblasts or factor VIII-positive endothelial cells. Mast cells did not appear to proliferate. Using a nuclease protection assay, we demonstrated induction of SCF mRNA within 72 hours of reperfusion. Immunohistochemical studies demonstrated that a subset of macrophages was the source of SCF immunoreactivity in the infarcted myocardium. SCF protein was not found in endothelial cells and myofibroblasts. Intravascular tryptase-positive, FITC-avidin-positive, CD11b-negative mast cell precursors were noted in the area of healing and in the cardiac lymph after 48 to 72 hours of reperfusion.
Mast cells increase in number in areas of collagen deposition and PCNA expression after myocardial ischemia. The data provide evidence of mast cell precursor infiltration into the areas of cellular injury. SCF is induced in a subset of macrophages infiltrating the healing myocardium. We suggest an important role for SCF in promoting chemotaxis and growth of mast cell precursors in the healing heart.</description><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Cardiology. Vascular system</subject><subject>Cell Division</subject><subject>Cloning, Molecular</subject><subject>Collagen - biosynthesis</subject><subject>Coronary heart disease</subject><subject>Dogs</subject><subject>Endothelium, Vascular - metabolism</subject><subject>Endothelium, Vascular - pathology</subject><subject>Factor VIII - analysis</subject><subject>Female</subject><subject>Heart</subject><subject>Male</subject><subject>Mast Cells - metabolism</subject><subject>Mast Cells - pathology</subject><subject>Medical sciences</subject><subject>Myocardial Infarction - metabolism</subject><subject>Myocardial Infarction - pathology</subject><subject>Myocardial Ischemia - metabolism</subject><subject>Myocardial Ischemia - pathology</subject><subject>Myocardial Reperfusion</subject><subject>Polymerase Chain Reaction</subject><subject>Proliferating Cell Nuclear Antigen - analysis</subject><subject>Proliferating Cell Nuclear Antigen - biosynthesis</subject><subject>Recombinant Proteins - biosynthesis</subject><subject>Stem Cell Factor - biosynthesis</subject><subject>Time Factors</subject><issn>0009-7322</issn><issn>1524-4539</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1998</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpdkUlrHDEQhUVIcMZOzjkFRAi5dVtLa-ljGLIYDIEsZ1EjVWOZXiZaCP73UTKDDz4Vxfvq8aRHyBvOes41v2a8399870fbm15b84zsuBJDNyg5Pic7xtjYGSnES3KZ831btTTqglyMhiurxY7UHwUX6nGe6QS-bInGNVRf4rbSmCnkvPkIBQP9E8sdXSCXEw3e16XO8J-EqWCiHta4Il0eNg8pRJibg7_DJQKFNdCER0xTze3gFXkxwZzx9XlekV-fP_3cf-1uv3252X-87fxgVOnkoLiSweiDsUFINllEeRgG9AZDe6FRqEdhD1zLsUnKerATKmaDFEGLUV6RDyffY9p-V8zFLS1Siw8rbjU7I61mRqoGvnsC3m81rS2bE1wYyayRDbo-QT5tOSec3DHFBdKD48z9a8Mx7lobbrTOuNZGu3h7tq2HBcMjf_7-pr8_65A9zFOC1cf8iAmpjeVW_gV1RJMB</recordid><startdate>19980818</startdate><enddate>19980818</enddate><creator>FRANGOGIANNIS, N. G</creator><creator>PERRARD, J. L</creator><creator>MENDOZA, L. H</creator><creator>BURNS, A. R</creator><creator>LINDSEY, M. L</creator><creator>BALLANTYNE, C. M</creator><creator>MICHAEL, L. H</creator><creator>SMITH, C. W</creator><creator>ENTMAN, M. L</creator><general>Lippincott Williams & Wilkins</general><general>American Heart Association, Inc</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>K9.</scope><scope>NAPCQ</scope><scope>U9A</scope><scope>7X8</scope></search><sort><creationdate>19980818</creationdate><title>Stem cell factor induction is associated with mast cell accumulation after canine myocardial ischemia and reperfusion</title><author>FRANGOGIANNIS, N. G ; PERRARD, J. L ; MENDOZA, L. H ; BURNS, A. R ; LINDSEY, M. L ; BALLANTYNE, C. M ; MICHAEL, L. H ; SMITH, C. W ; ENTMAN, M. L</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c475t-345153d76b78d230f8ee3b44ec7ed53975e6928b16398ee58ca8fe508d32d6293</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1998</creationdate><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Cardiology. Vascular system</topic><topic>Cell Division</topic><topic>Cloning, Molecular</topic><topic>Collagen - biosynthesis</topic><topic>Coronary heart disease</topic><topic>Dogs</topic><topic>Endothelium, Vascular - metabolism</topic><topic>Endothelium, Vascular - pathology</topic><topic>Factor VIII - analysis</topic><topic>Female</topic><topic>Heart</topic><topic>Male</topic><topic>Mast Cells - metabolism</topic><topic>Mast Cells - pathology</topic><topic>Medical sciences</topic><topic>Myocardial Infarction - metabolism</topic><topic>Myocardial Infarction - pathology</topic><topic>Myocardial Ischemia - metabolism</topic><topic>Myocardial Ischemia - pathology</topic><topic>Myocardial Reperfusion</topic><topic>Polymerase Chain Reaction</topic><topic>Proliferating Cell Nuclear Antigen - analysis</topic><topic>Proliferating Cell Nuclear Antigen - biosynthesis</topic><topic>Recombinant Proteins - biosynthesis</topic><topic>Stem Cell Factor - biosynthesis</topic><topic>Time Factors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>FRANGOGIANNIS, N. G</creatorcontrib><creatorcontrib>PERRARD, J. L</creatorcontrib><creatorcontrib>MENDOZA, L. H</creatorcontrib><creatorcontrib>BURNS, A. R</creatorcontrib><creatorcontrib>LINDSEY, M. L</creatorcontrib><creatorcontrib>BALLANTYNE, C. M</creatorcontrib><creatorcontrib>MICHAEL, L. H</creatorcontrib><creatorcontrib>SMITH, C. W</creatorcontrib><creatorcontrib>ENTMAN, M. L</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Premium</collection><collection>MEDLINE - Academic</collection><jtitle>Circulation (New York, N.Y.)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>FRANGOGIANNIS, N. G</au><au>PERRARD, J. L</au><au>MENDOZA, L. H</au><au>BURNS, A. R</au><au>LINDSEY, M. L</au><au>BALLANTYNE, C. M</au><au>MICHAEL, L. H</au><au>SMITH, C. W</au><au>ENTMAN, M. L</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Stem cell factor induction is associated with mast cell accumulation after canine myocardial ischemia and reperfusion</atitle><jtitle>Circulation (New York, N.Y.)</jtitle><addtitle>Circulation</addtitle><date>1998-08-18</date><risdate>1998</risdate><volume>98</volume><issue>7</issue><spage>687</spage><epage>698</epage><pages>687-698</pages><issn>0009-7322</issn><eissn>1524-4539</eissn><coden>CIRCAZ</coden><abstract>Myocardial infarction is associated with an intense inflammatory reaction leading to healing and scar formation. Because mast cells are a significant source of fibrogenic factors, we investigated mast cell accumulation and regulation of stem cell factor (SCF), a potent growth and tactic factor for mast cells, in the healing myocardium.
Using a canine model of myocardial ischemia and reperfusion, we demonstrated a striking increase of mast cell numbers during the healing phase of a myocardial infarction. Mast cell numbers started increasing after 72 hours of reperfusion, showing maximum accumulation in areas of collagen deposition (12.0+/-2.6-fold increase; P<0.01) and proliferating cell nuclear antigen (PCNA) expression. The majority of proliferating cells were identified as alpha-smooth muscle actin-positive myofibroblasts or factor VIII-positive endothelial cells. Mast cells did not appear to proliferate. Using a nuclease protection assay, we demonstrated induction of SCF mRNA within 72 hours of reperfusion. Immunohistochemical studies demonstrated that a subset of macrophages was the source of SCF immunoreactivity in the infarcted myocardium. SCF protein was not found in endothelial cells and myofibroblasts. Intravascular tryptase-positive, FITC-avidin-positive, CD11b-negative mast cell precursors were noted in the area of healing and in the cardiac lymph after 48 to 72 hours of reperfusion.
Mast cells increase in number in areas of collagen deposition and PCNA expression after myocardial ischemia. The data provide evidence of mast cell precursor infiltration into the areas of cellular injury. SCF is induced in a subset of macrophages infiltrating the healing myocardium. We suggest an important role for SCF in promoting chemotaxis and growth of mast cell precursors in the healing heart.</abstract><cop>Hagerstown, MD</cop><pub>Lippincott Williams & Wilkins</pub><pmid>9715862</pmid><doi>10.1161/01.CIR.98.7.687</doi><tpages>12</tpages><oa>free_for_read</oa></addata></record> |
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| source | MEDLINE; American Heart Association Journals; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Journals@Ovid Ovid Autoload |
| subjects | Animals Biological and medical sciences Cardiology. Vascular system Cell Division Cloning, Molecular Collagen - biosynthesis Coronary heart disease Dogs Endothelium, Vascular - metabolism Endothelium, Vascular - pathology Factor VIII - analysis Female Heart Male Mast Cells - metabolism Mast Cells - pathology Medical sciences Myocardial Infarction - metabolism Myocardial Infarction - pathology Myocardial Ischemia - metabolism Myocardial Ischemia - pathology Myocardial Reperfusion Polymerase Chain Reaction Proliferating Cell Nuclear Antigen - analysis Proliferating Cell Nuclear Antigen - biosynthesis Recombinant Proteins - biosynthesis Stem Cell Factor - biosynthesis Time Factors |
| title | Stem cell factor induction is associated with mast cell accumulation after canine myocardial ischemia and reperfusion |
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