Cyclophilin A is an inflammatory mediator that promotes atherosclerosis in apolipoprotein E-deficient mice
Cyclophilin A (CyPA; encoded by Ppia) is a ubiquitously expressed protein secreted in response to inflammatory stimuli. CyPA stimulates vascular smooth muscle cell migration and proliferation, endothelial cell adhesion molecule expression, and inflammatory cell chemotaxis. Given these activities, we...
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| Veröffentlicht in: | The Journal of experimental medicine 2011-01, Vol.208 (1), p.53-66 |
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| container_title | The Journal of experimental medicine |
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| creator | Nigro, Patrizia Satoh, Kimio O'Dell, Michael R Soe, Nwe Nwe Cui, Zhaoqiang Mohan, Amy Abe, Jun-ichi Alexis, Jeffrey D Sparks, Janet D Berk, Bradford C |
| description | Cyclophilin A (CyPA; encoded by Ppia) is a ubiquitously expressed protein secreted in response to inflammatory stimuli. CyPA stimulates vascular smooth muscle cell migration and proliferation, endothelial cell adhesion molecule expression, and inflammatory cell chemotaxis. Given these activities, we hypothesized that CyPA would promote atherosclerosis. Apolipoprotein E-deficient (Apoe(-/-)) mice fed a high-cholesterol diet for 16 wk developed more severe atherosclerosis compared with Apoe(-/-)Ppia(-/-) mice. Moreover, CyPA deficiency was associated with decreased low-density lipoprotein uptake, VCAM-1 (vascular cell adhesion molecule 1) expression, apoptosis, and increased eNOS (endothelial nitric oxide synthase) expression. To understand the vascular role of CyPA in atherosclerosis development, bone marrow (BM) cell transplantation was performed. Atherosclerosis was greater in Apoe(-/-) mice compared with Apoe(-/-)Ppia(-/-) mice after reconstitution with CyPA(+/+) BM cells, indicating that vascular-derived CyPA plays a crucial role in the progression of atherosclerosis. These data define a role for CyPA in atherosclerosis and suggest CyPA as a target for cardiovascular therapies. |
| doi_str_mv | 10.1084/jem.20101174 |
| format | Article |
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CyPA stimulates vascular smooth muscle cell migration and proliferation, endothelial cell adhesion molecule expression, and inflammatory cell chemotaxis. Given these activities, we hypothesized that CyPA would promote atherosclerosis. Apolipoprotein E-deficient (Apoe(-/-)) mice fed a high-cholesterol diet for 16 wk developed more severe atherosclerosis compared with Apoe(-/-)Ppia(-/-) mice. Moreover, CyPA deficiency was associated with decreased low-density lipoprotein uptake, VCAM-1 (vascular cell adhesion molecule 1) expression, apoptosis, and increased eNOS (endothelial nitric oxide synthase) expression. To understand the vascular role of CyPA in atherosclerosis development, bone marrow (BM) cell transplantation was performed. Atherosclerosis was greater in Apoe(-/-) mice compared with Apoe(-/-)Ppia(-/-) mice after reconstitution with CyPA(+/+) BM cells, indicating that vascular-derived CyPA plays a crucial role in the progression of atherosclerosis. These data define a role for CyPA in atherosclerosis and suggest CyPA as a target for cardiovascular therapies.</description><identifier>ISSN: 0022-1007</identifier><identifier>EISSN: 1540-9538</identifier><identifier>DOI: 10.1084/jem.20101174</identifier><identifier>PMID: 21173104</identifier><language>eng</language><publisher>United States: The Rockefeller University Press</publisher><subject>Animals ; Apolipoproteins E - deficiency ; Apolipoproteins E - metabolism ; Atherosclerosis - immunology ; Atherosclerosis - metabolism ; Atherosclerosis - pathology ; Cell Movement ; Cyclophilin A - genetics ; Cyclophilin A - metabolism ; Macrophages - cytology ; Macrophages - immunology ; Mice ; Mice, Knockout ; Nitric Oxide Synthase Type III - metabolism ; Reactive Oxygen Species - metabolism ; RNA, Small Interfering - genetics</subject><ispartof>The Journal of experimental medicine, 2011-01, Vol.208 (1), p.53-66</ispartof><rights>2011 Nigro et al. 2011</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c415t-64e2a8be643c6f0805bfd315daf94affcfad47088a7ae41a08d775ee989f66f3</citedby><cites>FETCH-LOGICAL-c415t-64e2a8be643c6f0805bfd315daf94affcfad47088a7ae41a08d775ee989f66f3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,777,781,882,27905,27906</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/21173104$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Nigro, Patrizia</creatorcontrib><creatorcontrib>Satoh, Kimio</creatorcontrib><creatorcontrib>O'Dell, Michael R</creatorcontrib><creatorcontrib>Soe, Nwe Nwe</creatorcontrib><creatorcontrib>Cui, Zhaoqiang</creatorcontrib><creatorcontrib>Mohan, Amy</creatorcontrib><creatorcontrib>Abe, Jun-ichi</creatorcontrib><creatorcontrib>Alexis, Jeffrey D</creatorcontrib><creatorcontrib>Sparks, Janet D</creatorcontrib><creatorcontrib>Berk, Bradford C</creatorcontrib><title>Cyclophilin A is an inflammatory mediator that promotes atherosclerosis in apolipoprotein E-deficient mice</title><title>The Journal of experimental medicine</title><addtitle>J Exp Med</addtitle><description>Cyclophilin A (CyPA; encoded by Ppia) is a ubiquitously expressed protein secreted in response to inflammatory stimuli. CyPA stimulates vascular smooth muscle cell migration and proliferation, endothelial cell adhesion molecule expression, and inflammatory cell chemotaxis. Given these activities, we hypothesized that CyPA would promote atherosclerosis. Apolipoprotein E-deficient (Apoe(-/-)) mice fed a high-cholesterol diet for 16 wk developed more severe atherosclerosis compared with Apoe(-/-)Ppia(-/-) mice. Moreover, CyPA deficiency was associated with decreased low-density lipoprotein uptake, VCAM-1 (vascular cell adhesion molecule 1) expression, apoptosis, and increased eNOS (endothelial nitric oxide synthase) expression. To understand the vascular role of CyPA in atherosclerosis development, bone marrow (BM) cell transplantation was performed. Atherosclerosis was greater in Apoe(-/-) mice compared with Apoe(-/-)Ppia(-/-) mice after reconstitution with CyPA(+/+) BM cells, indicating that vascular-derived CyPA plays a crucial role in the progression of atherosclerosis. These data define a role for CyPA in atherosclerosis and suggest CyPA as a target for cardiovascular therapies.</description><subject>Animals</subject><subject>Apolipoproteins E - deficiency</subject><subject>Apolipoproteins E - metabolism</subject><subject>Atherosclerosis - immunology</subject><subject>Atherosclerosis - metabolism</subject><subject>Atherosclerosis - pathology</subject><subject>Cell Movement</subject><subject>Cyclophilin A - genetics</subject><subject>Cyclophilin A - metabolism</subject><subject>Macrophages - cytology</subject><subject>Macrophages - immunology</subject><subject>Mice</subject><subject>Mice, Knockout</subject><subject>Nitric Oxide Synthase Type III - metabolism</subject><subject>Reactive Oxygen Species - metabolism</subject><subject>RNA, Small Interfering - genetics</subject><issn>0022-1007</issn><issn>1540-9538</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2011</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkU1r3DAQhkVpabZpbzkH33qJ05El29IlEJakLQR6yV3MyqOsFtlyLG1g_3205IP21MtoBj3zzkgvY2ccLjko-WNH42UDHDjv5Qe24q2EWrdCfWQrgKapOUB_wr6ktAPgUrbdZ3bSFFhwkCu2Wx9siPPWBz9V15VPFU6Vn1zAccQcl0M10uCPWZW3mKt5iWPMVLC8pSUmG46xtJV2nGPwcyxIplLe1AM5bz1NuRq9pa_sk8OQ6Nvrecrub2_u17_quz8_f6-v72oreZvrTlKDakOdFLZzoKDduEHwdkCnJTpnHQ6yB6WwR5IcQQ193xJppV3XOXHKrl5k5_2m7G7L-AWDmRc_4nIwEb3592byW_MQn4yARnAhi8D3V4ElPu4pZTP6ZCkEnCjuk9EgZaeE_j-pZCs017op5MULactvpYXc-z4czNFGU2w0bzYW_PzvN7zDb76JZ7rMnDE</recordid><startdate>20110117</startdate><enddate>20110117</enddate><creator>Nigro, Patrizia</creator><creator>Satoh, Kimio</creator><creator>O'Dell, Michael R</creator><creator>Soe, Nwe Nwe</creator><creator>Cui, Zhaoqiang</creator><creator>Mohan, Amy</creator><creator>Abe, Jun-ichi</creator><creator>Alexis, Jeffrey D</creator><creator>Sparks, Janet D</creator><creator>Berk, Bradford C</creator><general>The Rockefeller University Press</general><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>7X8</scope><scope>7T5</scope><scope>H94</scope><scope>5PM</scope></search><sort><creationdate>20110117</creationdate><title>Cyclophilin A is an inflammatory mediator that promotes atherosclerosis in apolipoprotein E-deficient mice</title><author>Nigro, Patrizia ; Satoh, Kimio ; O'Dell, Michael R ; Soe, Nwe Nwe ; Cui, Zhaoqiang ; Mohan, Amy ; Abe, Jun-ichi ; Alexis, Jeffrey D ; Sparks, Janet D ; Berk, Bradford C</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c415t-64e2a8be643c6f0805bfd315daf94affcfad47088a7ae41a08d775ee989f66f3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2011</creationdate><topic>Animals</topic><topic>Apolipoproteins E - deficiency</topic><topic>Apolipoproteins E - metabolism</topic><topic>Atherosclerosis - immunology</topic><topic>Atherosclerosis - metabolism</topic><topic>Atherosclerosis - pathology</topic><topic>Cell Movement</topic><topic>Cyclophilin A - genetics</topic><topic>Cyclophilin A - metabolism</topic><topic>Macrophages - cytology</topic><topic>Macrophages - immunology</topic><topic>Mice</topic><topic>Mice, Knockout</topic><topic>Nitric Oxide Synthase Type III - metabolism</topic><topic>Reactive Oxygen Species - metabolism</topic><topic>RNA, Small Interfering - genetics</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Nigro, Patrizia</creatorcontrib><creatorcontrib>Satoh, Kimio</creatorcontrib><creatorcontrib>O'Dell, Michael R</creatorcontrib><creatorcontrib>Soe, Nwe Nwe</creatorcontrib><creatorcontrib>Cui, Zhaoqiang</creatorcontrib><creatorcontrib>Mohan, Amy</creatorcontrib><creatorcontrib>Abe, Jun-ichi</creatorcontrib><creatorcontrib>Alexis, Jeffrey D</creatorcontrib><creatorcontrib>Sparks, Janet D</creatorcontrib><creatorcontrib>Berk, Bradford C</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>Immunology Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>The Journal of experimental medicine</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Nigro, Patrizia</au><au>Satoh, Kimio</au><au>O'Dell, Michael R</au><au>Soe, Nwe Nwe</au><au>Cui, Zhaoqiang</au><au>Mohan, Amy</au><au>Abe, Jun-ichi</au><au>Alexis, Jeffrey D</au><au>Sparks, Janet D</au><au>Berk, Bradford C</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Cyclophilin A is an inflammatory mediator that promotes atherosclerosis in apolipoprotein E-deficient mice</atitle><jtitle>The Journal of experimental medicine</jtitle><addtitle>J Exp Med</addtitle><date>2011-01-17</date><risdate>2011</risdate><volume>208</volume><issue>1</issue><spage>53</spage><epage>66</epage><pages>53-66</pages><issn>0022-1007</issn><eissn>1540-9538</eissn><abstract>Cyclophilin A (CyPA; encoded by Ppia) is a ubiquitously expressed protein secreted in response to inflammatory stimuli. CyPA stimulates vascular smooth muscle cell migration and proliferation, endothelial cell adhesion molecule expression, and inflammatory cell chemotaxis. Given these activities, we hypothesized that CyPA would promote atherosclerosis. Apolipoprotein E-deficient (Apoe(-/-)) mice fed a high-cholesterol diet for 16 wk developed more severe atherosclerosis compared with Apoe(-/-)Ppia(-/-) mice. Moreover, CyPA deficiency was associated with decreased low-density lipoprotein uptake, VCAM-1 (vascular cell adhesion molecule 1) expression, apoptosis, and increased eNOS (endothelial nitric oxide synthase) expression. To understand the vascular role of CyPA in atherosclerosis development, bone marrow (BM) cell transplantation was performed. Atherosclerosis was greater in Apoe(-/-) mice compared with Apoe(-/-)Ppia(-/-) mice after reconstitution with CyPA(+/+) BM cells, indicating that vascular-derived CyPA plays a crucial role in the progression of atherosclerosis. These data define a role for CyPA in atherosclerosis and suggest CyPA as a target for cardiovascular therapies.</abstract><cop>United States</cop><pub>The Rockefeller University Press</pub><pmid>21173104</pmid><doi>10.1084/jem.20101174</doi><tpages>14</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Animals Apolipoproteins E - deficiency Apolipoproteins E - metabolism Atherosclerosis - immunology Atherosclerosis - metabolism Atherosclerosis - pathology Cell Movement Cyclophilin A - genetics Cyclophilin A - metabolism Macrophages - cytology Macrophages - immunology Mice Mice, Knockout Nitric Oxide Synthase Type III - metabolism Reactive Oxygen Species - metabolism RNA, Small Interfering - genetics |
| title | Cyclophilin A is an inflammatory mediator that promotes atherosclerosis in apolipoprotein E-deficient mice |
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