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Fli1 deficiency contributes to the suppression of endothelial CXCL5 expression in systemic sclerosis
CXCL5 is a member of CXC chemokines with neutrophilic chemoattractant and pro-angiogenic properties, which has been implicated in the pathological angiogenesis of rheumatoid arthritis and inflammatory bowel diseases. Since aberrant angiogenesis is also involved in the developmental process of system...
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| Published in: | Archives of Dermatological Research 2014-05, Vol.306 (4), p.331-338 |
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| Main Authors: | , , , , , , , , , , , , , , |
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| container_title | Archives of Dermatological Research |
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| creator | Ichimura, Yohei Asano, Yoshihide Akamata, Kaname Takahashi, Takehiro Noda, Shinji Taniguchi, Takashi Toyama, Tetsuo Aozasa, Naohiko Sumida, Hayakazu Kuwano, Yoshihiro Yanaba, Koichi Tada, Yayoi Sugaya, Makoto Sato, Shinichi Kadono, Takafumi |
| description | CXCL5 is a member of CXC chemokines with neutrophilic chemoattractant and pro-angiogenic properties, which has been implicated in the pathological angiogenesis of rheumatoid arthritis and inflammatory bowel diseases. Since aberrant angiogenesis is also involved in the developmental process of systemic sclerosis (SSc), we herein measured serum CXCL5 levels in 63 SSc and 18 healthy subjects and investigated their clinical significance and the mechanism explaining altered expression of CXCL5 in SSc. Serum CXCL5 levels were significantly lower in SSc patients than in healthy subjects. In diffuse cutaneous SSc (dcSSc), serum CXCL5 levels were uniformly decreased in early stage ( |
| doi_str_mv | 10.1007/s00403-013-1431-9 |
| format | article |
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Since aberrant angiogenesis is also involved in the developmental process of systemic sclerosis (SSc), we herein measured serum CXCL5 levels in 63 SSc and 18 healthy subjects and investigated their clinical significance and the mechanism explaining altered expression of CXCL5 in SSc. Serum CXCL5 levels were significantly lower in SSc patients than in healthy subjects. In diffuse cutaneous SSc (dcSSc), serum CXCL5 levels were uniformly decreased in early stage (<1 year) and positively correlated with disease duration in patients with disease duration of <6 years. In non-early stage dcSSc (≥1 year), decreased serum CXCL5 levels were linked to the development of digital ulcers. Consistently, the expression levels of CXCL5 proteins were decreased in dermal blood vessels of early stage dcSSc. Importantly, Fli1 bound to the CXCL5 promoter and its gene silencing significantly suppressed the CXCL5 mRNA expression in human dermal microvascular endothelial cells. Furthermore, endothelial cell-specific Fli1 knockout mice, an animal model of SSc vasculopathy, exhibited decreased CXCL5 expression in dermal blood vessels. Collectively, these results indicate that CXCL5 is a member of angiogenesis-related genes, whose expression is suppressed at least partially due to Fli1 deficiency in SSc endothelial cells. Since Fli1 deficiency is deeply related to aberrant angiogenesis in SSc, it is plausible that serum CXCL5 levels inversely reflect the severity of SSc vasculopathy.</description><identifier>ISSN: 0340-3696</identifier><identifier>EISSN: 1432-069X</identifier><identifier>DOI: 10.1007/s00403-013-1431-9</identifier><identifier>PMID: 24292093</identifier><language>eng</language><publisher>Berlin/Heidelberg: Springer Berlin Heidelberg</publisher><subject>Aged ; Animals ; Cells, Cultured ; Chemokine CXCL5 - biosynthesis ; Chemokine CXCL5 - blood ; Chemokine CXCL5 - genetics ; Dermatology ; Endothelial Cells - metabolism ; Female ; Genetic Predisposition to Disease ; Humans ; Male ; Medicine ; Medicine & Public Health ; Mice ; Mice, Knockout ; Middle Aged ; Original Paper ; Promoter Regions, Genetic ; Proto-Oncogene Protein c-fli-1 - deficiency ; Proto-Oncogene Protein c-fli-1 - genetics ; RNA Interference ; RNA, Messenger - biosynthesis ; RNA, Small Interfering ; Scleroderma, Diffuse - blood</subject><ispartof>Archives of Dermatological Research, 2014-05, Vol.306 (4), p.331-338</ispartof><rights>Springer-Verlag Berlin Heidelberg 2013</rights><rights>Springer-Verlag Berlin Heidelberg 2014</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c438t-5fd03e2d8f4f07ca81a18b1a79fee2817a40d3ecce0aa7ab73f3751798ec47ee3</citedby><cites>FETCH-LOGICAL-c438t-5fd03e2d8f4f07ca81a18b1a79fee2817a40d3ecce0aa7ab73f3751798ec47ee3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/24292093$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Ichimura, Yohei</creatorcontrib><creatorcontrib>Asano, Yoshihide</creatorcontrib><creatorcontrib>Akamata, Kaname</creatorcontrib><creatorcontrib>Takahashi, Takehiro</creatorcontrib><creatorcontrib>Noda, Shinji</creatorcontrib><creatorcontrib>Taniguchi, Takashi</creatorcontrib><creatorcontrib>Toyama, Tetsuo</creatorcontrib><creatorcontrib>Aozasa, Naohiko</creatorcontrib><creatorcontrib>Sumida, Hayakazu</creatorcontrib><creatorcontrib>Kuwano, Yoshihiro</creatorcontrib><creatorcontrib>Yanaba, Koichi</creatorcontrib><creatorcontrib>Tada, Yayoi</creatorcontrib><creatorcontrib>Sugaya, Makoto</creatorcontrib><creatorcontrib>Sato, Shinichi</creatorcontrib><creatorcontrib>Kadono, Takafumi</creatorcontrib><title>Fli1 deficiency contributes to the suppression of endothelial CXCL5 expression in systemic sclerosis</title><title>Archives of Dermatological Research</title><addtitle>Arch Dermatol Res</addtitle><addtitle>Arch Dermatol Res</addtitle><description>CXCL5 is a member of CXC chemokines with neutrophilic chemoattractant and pro-angiogenic properties, which has been implicated in the pathological angiogenesis of rheumatoid arthritis and inflammatory bowel diseases. Since aberrant angiogenesis is also involved in the developmental process of systemic sclerosis (SSc), we herein measured serum CXCL5 levels in 63 SSc and 18 healthy subjects and investigated their clinical significance and the mechanism explaining altered expression of CXCL5 in SSc. Serum CXCL5 levels were significantly lower in SSc patients than in healthy subjects. In diffuse cutaneous SSc (dcSSc), serum CXCL5 levels were uniformly decreased in early stage (<1 year) and positively correlated with disease duration in patients with disease duration of <6 years. In non-early stage dcSSc (≥1 year), decreased serum CXCL5 levels were linked to the development of digital ulcers. Consistently, the expression levels of CXCL5 proteins were decreased in dermal blood vessels of early stage dcSSc. Importantly, Fli1 bound to the CXCL5 promoter and its gene silencing significantly suppressed the CXCL5 mRNA expression in human dermal microvascular endothelial cells. Furthermore, endothelial cell-specific Fli1 knockout mice, an animal model of SSc vasculopathy, exhibited decreased CXCL5 expression in dermal blood vessels. Collectively, these results indicate that CXCL5 is a member of angiogenesis-related genes, whose expression is suppressed at least partially due to Fli1 deficiency in SSc endothelial cells. Since Fli1 deficiency is deeply related to aberrant angiogenesis in SSc, it is plausible that serum CXCL5 levels inversely reflect the severity of SSc vasculopathy.</description><subject>Aged</subject><subject>Animals</subject><subject>Cells, Cultured</subject><subject>Chemokine CXCL5 - biosynthesis</subject><subject>Chemokine CXCL5 - blood</subject><subject>Chemokine CXCL5 - genetics</subject><subject>Dermatology</subject><subject>Endothelial Cells - metabolism</subject><subject>Female</subject><subject>Genetic Predisposition to Disease</subject><subject>Humans</subject><subject>Male</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Mice</subject><subject>Mice, Knockout</subject><subject>Middle Aged</subject><subject>Original Paper</subject><subject>Promoter Regions, Genetic</subject><subject>Proto-Oncogene Protein c-fli-1 - deficiency</subject><subject>Proto-Oncogene Protein c-fli-1 - genetics</subject><subject>RNA Interference</subject><subject>RNA, Messenger - biosynthesis</subject><subject>RNA, Small Interfering</subject><subject>Scleroderma, Diffuse - blood</subject><issn>0340-3696</issn><issn>1432-069X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2014</creationdate><recordtype>article</recordtype><recordid>eNp1kU1rGzEQhkVJaUyaH9BLEPSSy7ajD1vSsZikLRh6aSE3IWtHrcJ65Wh2If73Ueo0hELmomHmmXckvYx9EPBJAJjPBKBBdSBUJ7QSnXvDFi2RHazczQlbgNLQqZVbnbJzoltoYUBLMO_YqdTSSXBqwfrrIQveY8ox4xgPPJZxqnk7T0h8Knz6g5zm_b4iUS4jL4nj2JdWHnIY-PpmvVlyvH_u55HTgSbc5cgpDlgLZXrP3qYwEJ4_nWfs1_XVz_W3bvPj6_f1l00XtbJTt0w9KJS9TTqBicGKIOxWBOMSorTCBA29whgRQjBha1RSZimMsxi1QVRn7PKou6_lbkaa_C5TxGEII5aZvFgKZ5VRSjT043_obZnr2G73lwJplYVGiSMV2zuoYvL7mnehHrwA_-iCP7rgmwv-0QXv2szFk_K83WH_PPHvzxsgjwC11vgb64vVr6o-AD_6ksk</recordid><startdate>20140501</startdate><enddate>20140501</enddate><creator>Ichimura, Yohei</creator><creator>Asano, Yoshihide</creator><creator>Akamata, Kaname</creator><creator>Takahashi, Takehiro</creator><creator>Noda, Shinji</creator><creator>Taniguchi, Takashi</creator><creator>Toyama, Tetsuo</creator><creator>Aozasa, Naohiko</creator><creator>Sumida, Hayakazu</creator><creator>Kuwano, Yoshihiro</creator><creator>Yanaba, Koichi</creator><creator>Tada, Yayoi</creator><creator>Sugaya, Makoto</creator><creator>Sato, Shinichi</creator><creator>Kadono, Takafumi</creator><general>Springer Berlin Heidelberg</general><general>Springer Nature B.V</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>3V.</scope><scope>7T5</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>H94</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>7X8</scope></search><sort><creationdate>20140501</creationdate><title>Fli1 deficiency contributes to the suppression of endothelial CXCL5 expression in systemic sclerosis</title><author>Ichimura, Yohei ; 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Since aberrant angiogenesis is also involved in the developmental process of systemic sclerosis (SSc), we herein measured serum CXCL5 levels in 63 SSc and 18 healthy subjects and investigated their clinical significance and the mechanism explaining altered expression of CXCL5 in SSc. Serum CXCL5 levels were significantly lower in SSc patients than in healthy subjects. In diffuse cutaneous SSc (dcSSc), serum CXCL5 levels were uniformly decreased in early stage (<1 year) and positively correlated with disease duration in patients with disease duration of <6 years. In non-early stage dcSSc (≥1 year), decreased serum CXCL5 levels were linked to the development of digital ulcers. Consistently, the expression levels of CXCL5 proteins were decreased in dermal blood vessels of early stage dcSSc. Importantly, Fli1 bound to the CXCL5 promoter and its gene silencing significantly suppressed the CXCL5 mRNA expression in human dermal microvascular endothelial cells. Furthermore, endothelial cell-specific Fli1 knockout mice, an animal model of SSc vasculopathy, exhibited decreased CXCL5 expression in dermal blood vessels. Collectively, these results indicate that CXCL5 is a member of angiogenesis-related genes, whose expression is suppressed at least partially due to Fli1 deficiency in SSc endothelial cells. Since Fli1 deficiency is deeply related to aberrant angiogenesis in SSc, it is plausible that serum CXCL5 levels inversely reflect the severity of SSc vasculopathy.</abstract><cop>Berlin/Heidelberg</cop><pub>Springer Berlin Heidelberg</pub><pmid>24292093</pmid><doi>10.1007/s00403-013-1431-9</doi><tpages>8</tpages></addata></record> |
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| subjects | Aged Animals Cells, Cultured Chemokine CXCL5 - biosynthesis Chemokine CXCL5 - blood Chemokine CXCL5 - genetics Dermatology Endothelial Cells - metabolism Female Genetic Predisposition to Disease Humans Male Medicine Medicine & Public Health Mice Mice, Knockout Middle Aged Original Paper Promoter Regions, Genetic Proto-Oncogene Protein c-fli-1 - deficiency Proto-Oncogene Protein c-fli-1 - genetics RNA Interference RNA, Messenger - biosynthesis RNA, Small Interfering Scleroderma, Diffuse - blood |
| title | Fli1 deficiency contributes to the suppression of endothelial CXCL5 expression in systemic sclerosis |
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