Fractalkine and its receptor, CX3CR1, promote hypertensive interstitial fibrosis in the kidney
Hypertension promotes and escalates kidney injury, including kidney fibrosis. Fractalkine/CX3CL1 is a unique chemokine that works as a leukocyte chemoattractant and an adhesion molecule. Recently, fractalkine/CX3CL1 has been reported to promote tissue fibrosis via its cognate receptor, CX3CR1. Howev...
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| Veröffentlicht in: | Hypertension research 2011-06, Vol.34 (6), p.747-752 |
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| creator | Shimizu, Kazuaki Furuichi, Kengo Sakai, Norihiko Kitagawa, Kiyoki Matsushima, Kouji Mukaida, Naofumi Kaneko, Shuichi Wada, Takashi |
| description | Hypertension promotes and escalates kidney injury, including kidney fibrosis. Fractalkine/CX3CL1 is a unique chemokine that works as a leukocyte chemoattractant and an adhesion molecule. Recently, fractalkine/CX3CL1 has been reported to promote tissue fibrosis via its cognate receptor, CX3CR1. However, the involvement of the fractalkine-CX3CR1 axis in the pathogenesis of hypertensive kidney fibrosis remains unclear. The impacts of the fractalkine-CX3CR1 axis on hypertensive kidney fibrosis were investigated in a deoxycorticosterone acetate (DOCA)-salt hypertensive model in CX3CR1-deficient mice, which were sacrificed on day 28. The blood pressure levels were similarly elevated in both CX3CR1−/− C57BL/6 and wild-type C57BL/6 mice. Fractalkine and CX3CR1 were upregulated in kidneys that were damaged by hypertension. Deficiency in CX3CR1 inhibited kidney fibrosis, as evidenced by a decrease in the presence of interstitial fibrotic area detected by type I collagen in Mallory–Azan staining, concomitant with the downregulation of transforming growth factor (TGF)-β
1
and type I procollagen mRNA expression in damaged kidneys. The CX3CR1 blockade also decreased the number of infiltrating F4/80-positive macrophages in damaged kidneys. These results suggest that the fractalkine-CX3CR1 axis contributes to kidney fibrosis in a hypertensive mouse model, possibly by the upregulation of macrophage infiltration and the expression of TGF-β
1
and type I collagen. |
| doi_str_mv | 10.1038/hr.2011.23 |
| format | Article |
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1
and type I procollagen mRNA expression in damaged kidneys. The CX3CR1 blockade also decreased the number of infiltrating F4/80-positive macrophages in damaged kidneys. These results suggest that the fractalkine-CX3CR1 axis contributes to kidney fibrosis in a hypertensive mouse model, possibly by the upregulation of macrophage infiltration and the expression of TGF-β
1
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1
and type I procollagen mRNA expression in damaged kidneys. The CX3CR1 blockade also decreased the number of infiltrating F4/80-positive macrophages in damaged kidneys. These results suggest that the fractalkine-CX3CR1 axis contributes to kidney fibrosis in a hypertensive mouse model, possibly by the upregulation of macrophage infiltration and the expression of TGF-β
1
and type I collagen.</description><subject>631/250/127/98</subject><subject>692/420</subject><subject>692/699/1585</subject><subject>692/699/75/243</subject><subject>Animals</subject><subject>Antigens, Differentiation - analysis</subject><subject>Chemokine CX3CL1 - physiology</subject><subject>CX3C Chemokine Receptor 1</subject><subject>Desoxycorticosterone</subject><subject>Fibrosis</subject><subject>Geriatrics/Gerontology</subject><subject>Health Promotion and Disease Prevention</subject><subject>Hypertension - pathology</subject><subject>Internal Medicine</subject><subject>Kidney - pathology</subject><subject>Macrophages - immunology</subject><subject>Male</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Obstetrics/Perinatology/Midwifery</subject><subject>original-article</subject><subject>Public Health</subject><subject>Receptors, Chemokine - physiology</subject><subject>Signal Transduction</subject><subject>Transforming Growth Factor beta1 - analysis</subject><issn>0916-9636</issn><issn>1348-4214</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2011</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kF1LHDEUhkOp1K160x9QcldonTVf85HLsqgVBEEUvDJkkpNOdDazTTLC_nuzrHrZqwPnPDy850XoGyVLSnh3NsQlI5QuGf-EFpSLrhKMis9oQSRtKtnw5hB9TemJENbVkn5Bh-Vc05o1C_R4EbXJenz2AbAOFvuccAQDmzzFU7x64Ktbeoo3cVpPGfCw3UDMEJJ_AexDhpiyz16P2Pk-TsmnssV5APzsbYDtMTpwekxw8jaP0P3F-d3qT3V9c3m1-n1dmZqQXPVGyFYSw4Exa9tamNpxsIZYrXvTScukE71zrW462QNxjeCgbc2Z6xsiCD9CP_beEvTfDCmrtU8GxlEHmOakupbUom0lK-TPPWlK3BTBqU30ax23ihK1q1MNUe3qVIwX-Pubdu7XYD_Q9_4K8GsPpHIKfyGqp2mOobz6X13QeY7woRvijijAK0afie8</recordid><startdate>20110601</startdate><enddate>20110601</enddate><creator>Shimizu, Kazuaki</creator><creator>Furuichi, Kengo</creator><creator>Sakai, Norihiko</creator><creator>Kitagawa, Kiyoki</creator><creator>Matsushima, Kouji</creator><creator>Mukaida, Naofumi</creator><creator>Kaneko, Shuichi</creator><creator>Wada, Takashi</creator><general>Nature Publishing Group UK</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></search><sort><creationdate>20110601</creationdate><title>Fractalkine and its receptor, CX3CR1, promote hypertensive interstitial fibrosis in the kidney</title><author>Shimizu, Kazuaki ; Furuichi, Kengo ; Sakai, Norihiko ; Kitagawa, Kiyoki ; Matsushima, Kouji ; Mukaida, Naofumi ; Kaneko, Shuichi ; Wada, Takashi</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c500t-bc49790c3e22dd754c5f3edc0daabc89d29f4bff7a689be0f643ead532fb60403</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2011</creationdate><topic>631/250/127/98</topic><topic>692/420</topic><topic>692/699/1585</topic><topic>692/699/75/243</topic><topic>Animals</topic><topic>Antigens, Differentiation - analysis</topic><topic>Chemokine CX3CL1 - physiology</topic><topic>CX3C Chemokine Receptor 1</topic><topic>Desoxycorticosterone</topic><topic>Fibrosis</topic><topic>Geriatrics/Gerontology</topic><topic>Health Promotion and Disease Prevention</topic><topic>Hypertension - pathology</topic><topic>Internal Medicine</topic><topic>Kidney - pathology</topic><topic>Macrophages - immunology</topic><topic>Male</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Obstetrics/Perinatology/Midwifery</topic><topic>original-article</topic><topic>Public Health</topic><topic>Receptors, Chemokine - physiology</topic><topic>Signal Transduction</topic><topic>Transforming Growth Factor beta1 - analysis</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Shimizu, Kazuaki</creatorcontrib><creatorcontrib>Furuichi, Kengo</creatorcontrib><creatorcontrib>Sakai, Norihiko</creatorcontrib><creatorcontrib>Kitagawa, Kiyoki</creatorcontrib><creatorcontrib>Matsushima, Kouji</creatorcontrib><creatorcontrib>Mukaida, Naofumi</creatorcontrib><creatorcontrib>Kaneko, Shuichi</creatorcontrib><creatorcontrib>Wada, Takashi</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><jtitle>Hypertension research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Shimizu, Kazuaki</au><au>Furuichi, Kengo</au><au>Sakai, Norihiko</au><au>Kitagawa, Kiyoki</au><au>Matsushima, Kouji</au><au>Mukaida, Naofumi</au><au>Kaneko, Shuichi</au><au>Wada, Takashi</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Fractalkine and its receptor, CX3CR1, promote hypertensive interstitial fibrosis in the kidney</atitle><jtitle>Hypertension research</jtitle><stitle>Hypertens Res</stitle><addtitle>Hypertens Res</addtitle><date>2011-06-01</date><risdate>2011</risdate><volume>34</volume><issue>6</issue><spage>747</spage><epage>752</epage><pages>747-752</pages><issn>0916-9636</issn><eissn>1348-4214</eissn><abstract>Hypertension promotes and escalates kidney injury, including kidney fibrosis. Fractalkine/CX3CL1 is a unique chemokine that works as a leukocyte chemoattractant and an adhesion molecule. Recently, fractalkine/CX3CL1 has been reported to promote tissue fibrosis via its cognate receptor, CX3CR1. However, the involvement of the fractalkine-CX3CR1 axis in the pathogenesis of hypertensive kidney fibrosis remains unclear. The impacts of the fractalkine-CX3CR1 axis on hypertensive kidney fibrosis were investigated in a deoxycorticosterone acetate (DOCA)-salt hypertensive model in CX3CR1-deficient mice, which were sacrificed on day 28. The blood pressure levels were similarly elevated in both CX3CR1−/− C57BL/6 and wild-type C57BL/6 mice. Fractalkine and CX3CR1 were upregulated in kidneys that were damaged by hypertension. Deficiency in CX3CR1 inhibited kidney fibrosis, as evidenced by a decrease in the presence of interstitial fibrotic area detected by type I collagen in Mallory–Azan staining, concomitant with the downregulation of transforming growth factor (TGF)-β
1
and type I procollagen mRNA expression in damaged kidneys. The CX3CR1 blockade also decreased the number of infiltrating F4/80-positive macrophages in damaged kidneys. These results suggest that the fractalkine-CX3CR1 axis contributes to kidney fibrosis in a hypertensive mouse model, possibly by the upregulation of macrophage infiltration and the expression of TGF-β
1
and type I collagen.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>21451526</pmid><doi>10.1038/hr.2011.23</doi><tpages>6</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | 631/250/127/98 692/420 692/699/1585 692/699/75/243 Animals Antigens, Differentiation - analysis Chemokine CX3CL1 - physiology CX3C Chemokine Receptor 1 Desoxycorticosterone Fibrosis Geriatrics/Gerontology Health Promotion and Disease Prevention Hypertension - pathology Internal Medicine Kidney - pathology Macrophages - immunology Male Medicine Medicine & Public Health Mice Mice, Inbred C57BL Obstetrics/Perinatology/Midwifery original-article Public Health Receptors, Chemokine - physiology Signal Transduction Transforming Growth Factor beta1 - analysis |
| title | Fractalkine and its receptor, CX3CR1, promote hypertensive interstitial fibrosis in the kidney |
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