Expression of tenascin by vascular smooth muscle cells. Alterations in hypertensive rats and stimulation by angiotensin II
The extracellular matrix glycoprotein tenascin is associated with remodeling events in many embryonic and pathologic tissues. The expression of tenascin has been investigated by immunohistochemistry in blood vessels of Wistar-Kyoto (normotensive) and spontaneously hypertensive rats. Weak tenascin st...
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| Veröffentlicht in: | The American journal of pathology 1992-08, Vol.141 (2), p.377-388 |
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| creator | Mackie, EJ Scott-Burden, T Hahn, AW Kern, F Bernhardt, J Regenass, S Weller, A Buhler, FR |
| description | The extracellular matrix glycoprotein tenascin is associated with remodeling events in many embryonic and pathologic tissues. The expression of tenascin has been investigated by immunohistochemistry in blood vessels of Wistar-Kyoto (normotensive) and spontaneously hypertensive rats. Weak tenascin staining was present throughout the tunica media of large and small arteries from normotensive animals; strong staining was only detectable at branching sites. In arteries from hypertensive animals, foci of strong tenascin staining were scattered throughout the tunica media. The expression of tenascin mRNA and protein by rat aortic smooth muscle cells cultured in serum-free medium was induced by the vasoconstrictor peptide angiotensin II. Transforming growth factor-beta and platelet-derived growth factor also stimulated tenascin mRNA expression. Vascular smooth muscle cells attached specifically to a substratum of tenascin, but remained rounded. Thus, increased focal tenascin expression by vascular smooth muscle cells is associated with hypertension, and may mediate angiotensin II-induced changes in vascular structure in hypertension. |
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In arteries from hypertensive animals, foci of strong tenascin staining were scattered throughout the tunica media. The expression of tenascin mRNA and protein by rat aortic smooth muscle cells cultured in serum-free medium was induced by the vasoconstrictor peptide angiotensin II. Transforming growth factor-beta and platelet-derived growth factor also stimulated tenascin mRNA expression. Vascular smooth muscle cells attached specifically to a substratum of tenascin, but remained rounded. Thus, increased focal tenascin expression by vascular smooth muscle cells is associated with hypertension, and may mediate angiotensin II-induced changes in vascular structure in hypertension.</description><identifier>ISSN: 0002-9440</identifier><identifier>EISSN: 1525-2191</identifier><identifier>PMID: 1379781</identifier><identifier>CODEN: AJPAA4</identifier><language>eng</language><publisher>Bethesda, MD: ASIP</publisher><subject>Angiotensin II - pharmacology ; Animals ; Arterial hypertension. Arterial hypotension ; Arteries - metabolism ; Biological and medical sciences ; Blood and lymphatic vessels ; Cardiology. Vascular system ; Cell Adhesion - physiology ; Cell Adhesion Molecules, Neuronal - metabolism ; Cells, Cultured ; Extracellular Matrix Proteins - metabolism ; Hypertension - metabolism ; Hypertension - pathology ; Immunohistochemistry ; Male ; Medical sciences ; Muscle, Smooth, Vascular - metabolism ; Muscle, Smooth, Vascular - pathology ; Rats ; Rats, Inbred SHR ; Rats, Inbred WKY ; Reference Values ; Tenascin</subject><ispartof>The American journal of pathology, 1992-08, Vol.141 (2), p.377-388</ispartof><rights>1993 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC1886597/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC1886597/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,314,727,780,784,885,53791,53793</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=4384152$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/1379781$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Mackie, EJ</creatorcontrib><creatorcontrib>Scott-Burden, T</creatorcontrib><creatorcontrib>Hahn, AW</creatorcontrib><creatorcontrib>Kern, F</creatorcontrib><creatorcontrib>Bernhardt, J</creatorcontrib><creatorcontrib>Regenass, S</creatorcontrib><creatorcontrib>Weller, A</creatorcontrib><creatorcontrib>Buhler, FR</creatorcontrib><title>Expression of tenascin by vascular smooth muscle cells. Alterations in hypertensive rats and stimulation by angiotensin II</title><title>The American journal of pathology</title><addtitle>Am J Pathol</addtitle><description>The extracellular matrix glycoprotein tenascin is associated with remodeling events in many embryonic and pathologic tissues. The expression of tenascin has been investigated by immunohistochemistry in blood vessels of Wistar-Kyoto (normotensive) and spontaneously hypertensive rats. Weak tenascin staining was present throughout the tunica media of large and small arteries from normotensive animals; strong staining was only detectable at branching sites. In arteries from hypertensive animals, foci of strong tenascin staining were scattered throughout the tunica media. The expression of tenascin mRNA and protein by rat aortic smooth muscle cells cultured in serum-free medium was induced by the vasoconstrictor peptide angiotensin II. Transforming growth factor-beta and platelet-derived growth factor also stimulated tenascin mRNA expression. Vascular smooth muscle cells attached specifically to a substratum of tenascin, but remained rounded. Thus, increased focal tenascin expression by vascular smooth muscle cells is associated with hypertension, and may mediate angiotensin II-induced changes in vascular structure in hypertension.</description><subject>Angiotensin II - pharmacology</subject><subject>Animals</subject><subject>Arterial hypertension. Arterial hypotension</subject><subject>Arteries - metabolism</subject><subject>Biological and medical sciences</subject><subject>Blood and lymphatic vessels</subject><subject>Cardiology. Vascular system</subject><subject>Cell Adhesion - physiology</subject><subject>Cell Adhesion Molecules, Neuronal - metabolism</subject><subject>Cells, Cultured</subject><subject>Extracellular Matrix Proteins - metabolism</subject><subject>Hypertension - metabolism</subject><subject>Hypertension - pathology</subject><subject>Immunohistochemistry</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Muscle, Smooth, Vascular - metabolism</subject><subject>Muscle, Smooth, Vascular - pathology</subject><subject>Rats</subject><subject>Rats, Inbred SHR</subject><subject>Rats, Inbred WKY</subject><subject>Reference Values</subject><subject>Tenascin</subject><issn>0002-9440</issn><issn>1525-2191</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1992</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpVkc2O0zAUhSMEGsrAIyB5gdgF-dpuHW-QRqMBKo3EBtbWTeI0Hjl28E0K5elxoRpg5Z9z7nfk4yfVBrZiWwsw8LTacM5FbZTiz6sXRA_luJMNv6quQGqjG9hUP-9-zNkR-RRZGtjiIlLnI2tP7Fh2a8DMaEppGdm0Uhcc61wI9I7dhMVlXMocseIfT7PLZZr80bFyTwxjz2jxU0GcXWcixoNPv02R7fcvq2cDBnKvLut19fXD3ZfbT_X954_725v7epQClloMgqudAd3zVvWCa9N0sneDMFpDo51U4Lp2B2YwoNCJHrE3LWBnxLa8HOV19f4Pd17byfWdi0vGYOfsJ8wnm9Db_5XoR3tIRwtNs9saXQBvL4Ccvq2OFjt5OteA0aWVrJYAvJGyGF__m_QYcWm76G8ueqkWw5Axdp4ebUo2qvze37zRH8bvPjtLE4ZQoGDxYQYFVliptfwF_zGZ4Q</recordid><startdate>19920801</startdate><enddate>19920801</enddate><creator>Mackie, EJ</creator><creator>Scott-Burden, T</creator><creator>Hahn, AW</creator><creator>Kern, F</creator><creator>Bernhardt, J</creator><creator>Regenass, S</creator><creator>Weller, A</creator><creator>Buhler, FR</creator><general>ASIP</general><general>American Society for Investigative Pathology</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>19920801</creationdate><title>Expression of tenascin by vascular smooth muscle cells. Alterations in hypertensive rats and stimulation by angiotensin II</title><author>Mackie, EJ ; Scott-Burden, T ; Hahn, AW ; Kern, F ; Bernhardt, J ; Regenass, S ; Weller, A ; Buhler, FR</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-h321t-2f2046917d0b4d20798c3def2977187e341ecb619f914ae2daad9b1ac925440a3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1992</creationdate><topic>Angiotensin II - pharmacology</topic><topic>Animals</topic><topic>Arterial hypertension. Arterial hypotension</topic><topic>Arteries - metabolism</topic><topic>Biological and medical sciences</topic><topic>Blood and lymphatic vessels</topic><topic>Cardiology. Vascular system</topic><topic>Cell Adhesion - physiology</topic><topic>Cell Adhesion Molecules, Neuronal - metabolism</topic><topic>Cells, Cultured</topic><topic>Extracellular Matrix Proteins - metabolism</topic><topic>Hypertension - metabolism</topic><topic>Hypertension - pathology</topic><topic>Immunohistochemistry</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Muscle, Smooth, Vascular - metabolism</topic><topic>Muscle, Smooth, Vascular - pathology</topic><topic>Rats</topic><topic>Rats, Inbred SHR</topic><topic>Rats, Inbred WKY</topic><topic>Reference Values</topic><topic>Tenascin</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Mackie, EJ</creatorcontrib><creatorcontrib>Scott-Burden, T</creatorcontrib><creatorcontrib>Hahn, AW</creatorcontrib><creatorcontrib>Kern, F</creatorcontrib><creatorcontrib>Bernhardt, J</creatorcontrib><creatorcontrib>Regenass, S</creatorcontrib><creatorcontrib>Weller, A</creatorcontrib><creatorcontrib>Buhler, FR</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>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>The American journal of pathology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Mackie, EJ</au><au>Scott-Burden, T</au><au>Hahn, AW</au><au>Kern, F</au><au>Bernhardt, J</au><au>Regenass, S</au><au>Weller, A</au><au>Buhler, FR</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Expression of tenascin by vascular smooth muscle cells. Alterations in hypertensive rats and stimulation by angiotensin II</atitle><jtitle>The American journal of pathology</jtitle><addtitle>Am J Pathol</addtitle><date>1992-08-01</date><risdate>1992</risdate><volume>141</volume><issue>2</issue><spage>377</spage><epage>388</epage><pages>377-388</pages><issn>0002-9440</issn><eissn>1525-2191</eissn><coden>AJPAA4</coden><abstract>The extracellular matrix glycoprotein tenascin is associated with remodeling events in many embryonic and pathologic tissues. The expression of tenascin has been investigated by immunohistochemistry in blood vessels of Wistar-Kyoto (normotensive) and spontaneously hypertensive rats. Weak tenascin staining was present throughout the tunica media of large and small arteries from normotensive animals; strong staining was only detectable at branching sites. In arteries from hypertensive animals, foci of strong tenascin staining were scattered throughout the tunica media. The expression of tenascin mRNA and protein by rat aortic smooth muscle cells cultured in serum-free medium was induced by the vasoconstrictor peptide angiotensin II. Transforming growth factor-beta and platelet-derived growth factor also stimulated tenascin mRNA expression. Vascular smooth muscle cells attached specifically to a substratum of tenascin, but remained rounded. Thus, increased focal tenascin expression by vascular smooth muscle cells is associated with hypertension, and may mediate angiotensin II-induced changes in vascular structure in hypertension.</abstract><cop>Bethesda, MD</cop><pub>ASIP</pub><pmid>1379781</pmid><tpages>12</tpages></addata></record> |
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| subjects | Angiotensin II - pharmacology Animals Arterial hypertension. Arterial hypotension Arteries - metabolism Biological and medical sciences Blood and lymphatic vessels Cardiology. Vascular system Cell Adhesion - physiology Cell Adhesion Molecules, Neuronal - metabolism Cells, Cultured Extracellular Matrix Proteins - metabolism Hypertension - metabolism Hypertension - pathology Immunohistochemistry Male Medical sciences Muscle, Smooth, Vascular - metabolism Muscle, Smooth, Vascular - pathology Rats Rats, Inbred SHR Rats, Inbred WKY Reference Values Tenascin |
| title | Expression of tenascin by vascular smooth muscle cells. Alterations in hypertensive rats and stimulation by angiotensin II |
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