Cyclophilin A Is a Secreted Growth Factor Induced by Oxidative Stress
ABSTRACT—Reactive oxygen species have been implicated in the pathogenesis of atherosclerosis, hypertension, and restenosis, in part by promoting vascular smooth muscle cell (VSMC) growth. Many VSMC growth factors are secreted by VSMC and act in an autocrine manner. Here we demonstrate that cyclophil...
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| Veröffentlicht in: | Circulation research 2000-10, Vol.87 (9), p.789-796 |
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| creator | Jin, Zheng-Gen Melaragno, Matthew G Liao, Duan-Fang Yan, Chen Haendeler, Judith Suh, Young-Ah Lambeth, J David Berk, Bradford C |
| description | ABSTRACT—Reactive oxygen species have been implicated in the pathogenesis of atherosclerosis, hypertension, and restenosis, in part by promoting vascular smooth muscle cell (VSMC) growth. Many VSMC growth factors are secreted by VSMC and act in an autocrine manner. Here we demonstrate that cyclophilin A (CyPA), a member of the immunophilin family, is secreted by VSMCs in response to oxidative stress and mediates extracellular signal–regulated kinase (ERK1/2) activation and VSMC growth by reactive oxygen species. Human recombinant CyPA can mimic the effects of secreted CyPA to stimulate ERK1/2 and cell growth. The peptidyl-prolyl isomerase activity is required for ERK1/2 activation by CyPA. In vivo, CyPA expression and secretion are increased by oxidative stress and vascular injury. These findings are the first to identify CyPA as a secreted redox-sensitive mediator, establish CyPA as a VSMC growth factor, and suggest an important role for CyPA and enzymes with peptidyl-prolyl isomerase activity in the pathogenesis of vascular diseases. |
| doi_str_mv | 10.1161/01.res.87.9.789 |
| format | Article |
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Many VSMC growth factors are secreted by VSMC and act in an autocrine manner. Here we demonstrate that cyclophilin A (CyPA), a member of the immunophilin family, is secreted by VSMCs in response to oxidative stress and mediates extracellular signal–regulated kinase (ERK1/2) activation and VSMC growth by reactive oxygen species. Human recombinant CyPA can mimic the effects of secreted CyPA to stimulate ERK1/2 and cell growth. The peptidyl-prolyl isomerase activity is required for ERK1/2 activation by CyPA. In vivo, CyPA expression and secretion are increased by oxidative stress and vascular injury. These findings are the first to identify CyPA as a secreted redox-sensitive mediator, establish CyPA as a VSMC growth factor, and suggest an important role for CyPA and enzymes with peptidyl-prolyl isomerase activity in the pathogenesis of vascular diseases.</description><identifier>ISSN: 0009-7330</identifier><identifier>EISSN: 1524-4571</identifier><identifier>DOI: 10.1161/01.res.87.9.789</identifier><identifier>PMID: 11055983</identifier><identifier>CODEN: CIRUAL</identifier><language>eng</language><publisher>Hagerstown, MD: American Heart Association, Inc</publisher><subject>1,2-Dihydroxybenzene-3,5-Disulfonic Acid Disodium Salt - pharmacology ; Aminoquinolines - pharmacology ; Animals ; Apoptosis - drug effects ; Biological and medical sciences ; Blood and lymphatic vessels ; Cardiology. Vascular system ; Carotid Artery Injuries - metabolism ; Cell Division - drug effects ; Cyclophilin A - analysis ; Cyclophilin A - metabolism ; Enzyme Activation ; Enzyme Inhibitors - pharmacology ; Free Radical Scavengers - pharmacology ; Male ; Medical sciences ; Miscellaneous ; Mitogen-Activated Protein Kinase 3 ; Mitogen-Activated Protein Kinases - metabolism ; Muscle, Smooth, Vascular - cytology ; Muscle, Smooth, Vascular - metabolism ; NADH, NADPH Oxidoreductases - genetics ; NADH, NADPH Oxidoreductases - metabolism ; NADPH Oxidases ; Nitroprusside ; Onium Compounds - pharmacology ; Oxidative Stress ; Peptidylprolyl Isomerase ; Rats ; Rats, Sprague-Dawley ; Reactive Oxygen Species - metabolism ; Recombinant Proteins - metabolism ; Transfection ; Vascular Diseases - etiology</subject><ispartof>Circulation research, 2000-10, Vol.87 (9), p.789-796</ispartof><rights>2000 American Heart Association, Inc.</rights><rights>2001 INIST-CNRS</rights><rights>Copyright American Heart Association, Inc. 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Many VSMC growth factors are secreted by VSMC and act in an autocrine manner. Here we demonstrate that cyclophilin A (CyPA), a member of the immunophilin family, is secreted by VSMCs in response to oxidative stress and mediates extracellular signal–regulated kinase (ERK1/2) activation and VSMC growth by reactive oxygen species. Human recombinant CyPA can mimic the effects of secreted CyPA to stimulate ERK1/2 and cell growth. The peptidyl-prolyl isomerase activity is required for ERK1/2 activation by CyPA. In vivo, CyPA expression and secretion are increased by oxidative stress and vascular injury. These findings are the first to identify CyPA as a secreted redox-sensitive mediator, establish CyPA as a VSMC growth factor, and suggest an important role for CyPA and enzymes with peptidyl-prolyl isomerase activity in the pathogenesis of vascular diseases.</description><subject>1,2-Dihydroxybenzene-3,5-Disulfonic Acid Disodium Salt - pharmacology</subject><subject>Aminoquinolines - pharmacology</subject><subject>Animals</subject><subject>Apoptosis - drug effects</subject><subject>Biological and medical sciences</subject><subject>Blood and lymphatic vessels</subject><subject>Cardiology. Vascular system</subject><subject>Carotid Artery Injuries - metabolism</subject><subject>Cell Division - drug effects</subject><subject>Cyclophilin A - analysis</subject><subject>Cyclophilin A - metabolism</subject><subject>Enzyme Activation</subject><subject>Enzyme Inhibitors - pharmacology</subject><subject>Free Radical Scavengers - pharmacology</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Miscellaneous</subject><subject>Mitogen-Activated Protein Kinase 3</subject><subject>Mitogen-Activated Protein Kinases - metabolism</subject><subject>Muscle, Smooth, Vascular - cytology</subject><subject>Muscle, Smooth, Vascular - metabolism</subject><subject>NADH, NADPH Oxidoreductases - genetics</subject><subject>NADH, NADPH Oxidoreductases - metabolism</subject><subject>NADPH Oxidases</subject><subject>Nitroprusside</subject><subject>Onium Compounds - pharmacology</subject><subject>Oxidative Stress</subject><subject>Peptidylprolyl Isomerase</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Reactive Oxygen Species - metabolism</subject><subject>Recombinant Proteins - metabolism</subject><subject>Transfection</subject><subject>Vascular Diseases - etiology</subject><issn>0009-7330</issn><issn>1524-4571</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2000</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpd0c-LEzEUB_AgiltXz94kKHib2ZcfM0mOS-nuFhYWrJ5DkknorOlMTWas_e9NaVnBUx7hk5fH9yH0kUBNSEtugNTJ51qKWtVCqldoQRrKK94I8hotAEBVgjG4Qu9yfgYgnFH1Fl0RAk2jJFug1fLo4rjf9rEf8C1eZ2zwxrvkJ9_h-zQepi2-M24aE14P3ezKrT3ipz99Z6b-t8ebqfyf36M3wcTsP1zOa_TjbvV9-VA9Pt2vl7ePlWtYyyrmAmmUVQG49J2UbehaC6aVgnWdBeAQhHU-8GCNB2O84SIoa2XnWKuMY9fo67nvPo2_Zp8nveuz8zGawY9z1oIy0XBJCvz8H3we5zSU2TQllBPRKlrQzRm5NOacfND71O9MOmoC-hSvBqK_rTZaCq10ibe8-HRpO9ud7_75S54FfLkAk52JIZnB9fnFScqa9jQdP6vDGCef8s84H3zSW2_itNVla8CA0IqWggAVUJ0Kxv4CXsORWw</recordid><startdate>20001027</startdate><enddate>20001027</enddate><creator>Jin, Zheng-Gen</creator><creator>Melaragno, Matthew G</creator><creator>Liao, Duan-Fang</creator><creator>Yan, Chen</creator><creator>Haendeler, Judith</creator><creator>Suh, Young-Ah</creator><creator>Lambeth, J David</creator><creator>Berk, Bradford C</creator><general>American Heart Association, Inc</general><general>Lippincott</general><general>Lippincott Williams & Wilkins Ovid Technologies</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>7QP</scope><scope>7T5</scope><scope>7TK</scope><scope>H94</scope><scope>K9.</scope><scope>7X8</scope></search><sort><creationdate>20001027</creationdate><title>Cyclophilin A Is a Secreted Growth Factor Induced by Oxidative Stress</title><author>Jin, Zheng-Gen ; Melaragno, Matthew G ; Liao, Duan-Fang ; Yan, Chen ; Haendeler, Judith ; Suh, Young-Ah ; Lambeth, J David ; Berk, Bradford C</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5363-3cf159b9f048ed886fd6b0a6873ddb0040f7bcef4fbae0aaea47f9bb8dc369ac3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2000</creationdate><topic>1,2-Dihydroxybenzene-3,5-Disulfonic Acid Disodium Salt - pharmacology</topic><topic>Aminoquinolines - pharmacology</topic><topic>Animals</topic><topic>Apoptosis - drug effects</topic><topic>Biological and medical sciences</topic><topic>Blood and lymphatic vessels</topic><topic>Cardiology. Vascular system</topic><topic>Carotid Artery Injuries - metabolism</topic><topic>Cell Division - drug effects</topic><topic>Cyclophilin A - analysis</topic><topic>Cyclophilin A - metabolism</topic><topic>Enzyme Activation</topic><topic>Enzyme Inhibitors - pharmacology</topic><topic>Free Radical Scavengers - pharmacology</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Miscellaneous</topic><topic>Mitogen-Activated Protein Kinase 3</topic><topic>Mitogen-Activated Protein Kinases - metabolism</topic><topic>Muscle, Smooth, Vascular - cytology</topic><topic>Muscle, Smooth, Vascular - metabolism</topic><topic>NADH, NADPH Oxidoreductases - genetics</topic><topic>NADH, NADPH Oxidoreductases - metabolism</topic><topic>NADPH Oxidases</topic><topic>Nitroprusside</topic><topic>Onium Compounds - pharmacology</topic><topic>Oxidative Stress</topic><topic>Peptidylprolyl Isomerase</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Reactive Oxygen Species - metabolism</topic><topic>Recombinant Proteins - metabolism</topic><topic>Transfection</topic><topic>Vascular Diseases - etiology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Jin, Zheng-Gen</creatorcontrib><creatorcontrib>Melaragno, Matthew G</creatorcontrib><creatorcontrib>Liao, Duan-Fang</creatorcontrib><creatorcontrib>Yan, Chen</creatorcontrib><creatorcontrib>Haendeler, Judith</creatorcontrib><creatorcontrib>Suh, Young-Ah</creatorcontrib><creatorcontrib>Lambeth, J David</creatorcontrib><creatorcontrib>Berk, Bradford C</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>Calcium & Calcified Tissue Abstracts</collection><collection>Immunology Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>MEDLINE - Academic</collection><jtitle>Circulation research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Jin, Zheng-Gen</au><au>Melaragno, Matthew G</au><au>Liao, Duan-Fang</au><au>Yan, Chen</au><au>Haendeler, Judith</au><au>Suh, Young-Ah</au><au>Lambeth, J David</au><au>Berk, Bradford C</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Cyclophilin A Is a Secreted Growth Factor Induced by Oxidative Stress</atitle><jtitle>Circulation research</jtitle><addtitle>Circ Res</addtitle><date>2000-10-27</date><risdate>2000</risdate><volume>87</volume><issue>9</issue><spage>789</spage><epage>796</epage><pages>789-796</pages><issn>0009-7330</issn><eissn>1524-4571</eissn><coden>CIRUAL</coden><abstract>ABSTRACT—Reactive oxygen species have been implicated in the pathogenesis of atherosclerosis, hypertension, and restenosis, in part by promoting vascular smooth muscle cell (VSMC) growth. Many VSMC growth factors are secreted by VSMC and act in an autocrine manner. Here we demonstrate that cyclophilin A (CyPA), a member of the immunophilin family, is secreted by VSMCs in response to oxidative stress and mediates extracellular signal–regulated kinase (ERK1/2) activation and VSMC growth by reactive oxygen species. Human recombinant CyPA can mimic the effects of secreted CyPA to stimulate ERK1/2 and cell growth. The peptidyl-prolyl isomerase activity is required for ERK1/2 activation by CyPA. In vivo, CyPA expression and secretion are increased by oxidative stress and vascular injury. These findings are the first to identify CyPA as a secreted redox-sensitive mediator, establish CyPA as a VSMC growth factor, and suggest an important role for CyPA and enzymes with peptidyl-prolyl isomerase activity in the pathogenesis of vascular diseases.</abstract><cop>Hagerstown, MD</cop><pub>American Heart Association, Inc</pub><pmid>11055983</pmid><doi>10.1161/01.res.87.9.789</doi><tpages>8</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | 1,2-Dihydroxybenzene-3,5-Disulfonic Acid Disodium Salt - pharmacology Aminoquinolines - pharmacology Animals Apoptosis - drug effects Biological and medical sciences Blood and lymphatic vessels Cardiology. Vascular system Carotid Artery Injuries - metabolism Cell Division - drug effects Cyclophilin A - analysis Cyclophilin A - metabolism Enzyme Activation Enzyme Inhibitors - pharmacology Free Radical Scavengers - pharmacology Male Medical sciences Miscellaneous Mitogen-Activated Protein Kinase 3 Mitogen-Activated Protein Kinases - metabolism Muscle, Smooth, Vascular - cytology Muscle, Smooth, Vascular - metabolism NADH, NADPH Oxidoreductases - genetics NADH, NADPH Oxidoreductases - metabolism NADPH Oxidases Nitroprusside Onium Compounds - pharmacology Oxidative Stress Peptidylprolyl Isomerase Rats Rats, Sprague-Dawley Reactive Oxygen Species - metabolism Recombinant Proteins - metabolism Transfection Vascular Diseases - etiology |
| title | Cyclophilin A Is a Secreted Growth Factor Induced by Oxidative Stress |
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