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Enhanced MCP-1 release by keloid CD14+ cells augments fibroblast proliferation: role of MCP-1 and Akt pathway in keloids

Please cite this paper as: Enhanced MCP‐1 release by keloid CD14+ cells augments fibroblast proliferation: role of MCP‐1 and Akt pathway in keloids. Experimental Dermatology 2010; 19: e142–e150. :  Keloids are fibrous overgrowth induced by cutaneous injury. The pathogenesis of keloids is poorly unde...

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Published in:Experimental dermatology 2010-08, Vol.19 (8), p.e142-e150
Main Authors: Liao, Wei-Ting, Yu, Hsin-Su, Arbiser, Jack L., Hong, Chein-Hui, Govindarajan, Baskaran, Chai, Chih-Yin, Shan, Wan-Ju, Lin, Yu-Fen, Chen, Gwo-Shing, Lee, Chih-Hung
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cited_by cdi_FETCH-LOGICAL-c4561-b85139b8e8ed5720552e6c4e5b74a43f54a7ddb000e6ed1448b33c19a7291c283
cites cdi_FETCH-LOGICAL-c4561-b85139b8e8ed5720552e6c4e5b74a43f54a7ddb000e6ed1448b33c19a7291c283
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creator Liao, Wei-Ting
Yu, Hsin-Su
Arbiser, Jack L.
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Govindarajan, Baskaran
Chai, Chih-Yin
Shan, Wan-Ju
Lin, Yu-Fen
Chen, Gwo-Shing
Lee, Chih-Hung
description Please cite this paper as: Enhanced MCP‐1 release by keloid CD14+ cells augments fibroblast proliferation: role of MCP‐1 and Akt pathway in keloids. Experimental Dermatology 2010; 19: e142–e150. :  Keloids are fibrous overgrowth induced by cutaneous injury. The pathogenesis of keloids is poorly understood, and no convincing animal model exists. Current hypotheses of the pathogenesis classify keloids as an entity of aberrant fibrosis. Hyperactivation of the MCP‐1/CCR2 axis reportedly causes fibrosis in liver cirrhosis, atherosclerosis and lung fibrosis. Circulating CD14+ monocytes are precursors of circulating fibrocytes and contribute to fibrogenesis by a MCP‐1/CCR2‐dependent loop. As there is an increase in monocyte lineages in keloids, the aim of this study is to determine whether peripheral CD14+ monocytes in keloid patients trigger fibroblast proliferation through MCP‐1. Expressions of MCP‐1 and its receptor CCR2 in keloid lesions were measured by immunohistochemistry and real‐time PCR. The results revealed an increase in MCP‐1 and CCR2 in the keloid tissues. Co‐culture of keloid CD14+ cells and normal fibroblasts enhanced fibroblast proliferation and a parallel increase in extracellular MCP‐1. We further found that MCP‐1 modest enhanced fibroblast proliferation via Akt activation. Blockade of either MCP‐1 or Akt signaling suppressed the mediation of fibroblast proliferation by CD14+ cells from patients. These results demonstrated that enhanced MCP‐1 release by keloid CD14+ cells augments fibroblast proliferation via Akt pathway in keloids. We concluded that enhanced MCP‐1 release by keloid CD14+ cells augments fibroblast proliferation, which might initiate keloid development.
doi_str_mv 10.1111/j.1600-0625.2009.01021.x
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Experimental Dermatology 2010; 19: e142–e150. :  Keloids are fibrous overgrowth induced by cutaneous injury. The pathogenesis of keloids is poorly understood, and no convincing animal model exists. Current hypotheses of the pathogenesis classify keloids as an entity of aberrant fibrosis. Hyperactivation of the MCP‐1/CCR2 axis reportedly causes fibrosis in liver cirrhosis, atherosclerosis and lung fibrosis. Circulating CD14+ monocytes are precursors of circulating fibrocytes and contribute to fibrogenesis by a MCP‐1/CCR2‐dependent loop. As there is an increase in monocyte lineages in keloids, the aim of this study is to determine whether peripheral CD14+ monocytes in keloid patients trigger fibroblast proliferation through MCP‐1. Expressions of MCP‐1 and its receptor CCR2 in keloid lesions were measured by immunohistochemistry and real‐time PCR. The results revealed an increase in MCP‐1 and CCR2 in the keloid tissues. Co‐culture of keloid CD14+ cells and normal fibroblasts enhanced fibroblast proliferation and a parallel increase in extracellular MCP‐1. We further found that MCP‐1 modest enhanced fibroblast proliferation via Akt activation. Blockade of either MCP‐1 or Akt signaling suppressed the mediation of fibroblast proliferation by CD14+ cells from patients. These results demonstrated that enhanced MCP‐1 release by keloid CD14+ cells augments fibroblast proliferation via Akt pathway in keloids. We concluded that enhanced MCP‐1 release by keloid CD14+ cells augments fibroblast proliferation, which might initiate keloid development.</description><identifier>ISSN: 0906-6705</identifier><identifier>EISSN: 1600-0625</identifier><identifier>DOI: 10.1111/j.1600-0625.2009.01021.x</identifier><identifier>PMID: 20100200</identifier><language>eng</language><publisher>Oxford, UK: Blackwell Publishing Ltd</publisher><subject>Adolescent ; Adult ; Akt ; Case-Control Studies ; Cell Proliferation ; Cells, Cultured ; Chemokine CCL2 - metabolism ; Coculture Techniques ; Female ; fibroblast proliferation ; Fibroblasts - pathology ; Humans ; keloid ; Keloid - metabolism ; Lipopolysaccharide Receptors - metabolism ; Male ; MCP-1 ; Monocytes - immunology ; Monocytes - pathology ; monocytes/macrophages ; Proto-Oncogene Proteins c-akt - metabolism ; Receptors, CCR2 - metabolism ; Signal Transduction - physiology ; Young Adult</subject><ispartof>Experimental dermatology, 2010-08, Vol.19 (8), p.e142-e150</ispartof><rights>2009 John Wiley &amp; Sons A/S</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4561-b85139b8e8ed5720552e6c4e5b74a43f54a7ddb000e6ed1448b33c19a7291c283</citedby><cites>FETCH-LOGICAL-c4561-b85139b8e8ed5720552e6c4e5b74a43f54a7ddb000e6ed1448b33c19a7291c283</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/20100200$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Liao, Wei-Ting</creatorcontrib><creatorcontrib>Yu, Hsin-Su</creatorcontrib><creatorcontrib>Arbiser, Jack L.</creatorcontrib><creatorcontrib>Hong, Chein-Hui</creatorcontrib><creatorcontrib>Govindarajan, Baskaran</creatorcontrib><creatorcontrib>Chai, Chih-Yin</creatorcontrib><creatorcontrib>Shan, Wan-Ju</creatorcontrib><creatorcontrib>Lin, Yu-Fen</creatorcontrib><creatorcontrib>Chen, Gwo-Shing</creatorcontrib><creatorcontrib>Lee, Chih-Hung</creatorcontrib><title>Enhanced MCP-1 release by keloid CD14+ cells augments fibroblast proliferation: role of MCP-1 and Akt pathway in keloids</title><title>Experimental dermatology</title><addtitle>Exp Dermatol</addtitle><description>Please cite this paper as: Enhanced MCP‐1 release by keloid CD14+ cells augments fibroblast proliferation: role of MCP‐1 and Akt pathway in keloids. 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Co‐culture of keloid CD14+ cells and normal fibroblasts enhanced fibroblast proliferation and a parallel increase in extracellular MCP‐1. We further found that MCP‐1 modest enhanced fibroblast proliferation via Akt activation. Blockade of either MCP‐1 or Akt signaling suppressed the mediation of fibroblast proliferation by CD14+ cells from patients. These results demonstrated that enhanced MCP‐1 release by keloid CD14+ cells augments fibroblast proliferation via Akt pathway in keloids. We concluded that enhanced MCP‐1 release by keloid CD14+ cells augments fibroblast proliferation, which might initiate keloid development.</description><subject>Adolescent</subject><subject>Adult</subject><subject>Akt</subject><subject>Case-Control Studies</subject><subject>Cell Proliferation</subject><subject>Cells, Cultured</subject><subject>Chemokine CCL2 - metabolism</subject><subject>Coculture Techniques</subject><subject>Female</subject><subject>fibroblast proliferation</subject><subject>Fibroblasts - pathology</subject><subject>Humans</subject><subject>keloid</subject><subject>Keloid - metabolism</subject><subject>Lipopolysaccharide Receptors - metabolism</subject><subject>Male</subject><subject>MCP-1</subject><subject>Monocytes - immunology</subject><subject>Monocytes - pathology</subject><subject>monocytes/macrophages</subject><subject>Proto-Oncogene Proteins c-akt - metabolism</subject><subject>Receptors, CCR2 - metabolism</subject><subject>Signal Transduction - physiology</subject><subject>Young Adult</subject><issn>0906-6705</issn><issn>1600-0625</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2010</creationdate><recordtype>article</recordtype><recordid>eNqNkcuO0zAYhS0EYsrAKyDvWKCE3_EtQWIx6pSCKDdpuOwsO_nDuE2TwU417dvj0NI12TiWv3NsfyaEMshZ-l6tc6YAMlCFzAuAKgcGBcv3D8jsvPCQzKAClSkN8oI8iXENwDTX8jG5KBIPKTgj-0V_a_saG_px_iVjNGCHNiJ1B7rBbvANnV8z8ZLW2HWR2t2vLfZjpK13YXCdjSO9C0PnWwx29EP_mqYZ0qE91dm-oVebBNnx9t4eqO9PtfEpedTaLuKz03hJvr1d3MzfZavPy_fzq1VWC6lY5krJeOVKLLGRugApC1S1QOm0sIK3UljdNA4AUGHDhCgd5zWrrC4qVhclvyQvjr3pnL93GEez9XG6je1x2EWjuUgCudaJLI9kHYYYA7bmLvitDQfDwEzazdpMds1k10zazV_tZp-iz0-b7NwWm3Pwn-cEvDkC977Dw38Xm8XP6-kv5bNj3scR9-e8DRujpjc1Pz4tzc3yQ6lW37n5yv8ADYSduQ</recordid><startdate>201008</startdate><enddate>201008</enddate><creator>Liao, Wei-Ting</creator><creator>Yu, Hsin-Su</creator><creator>Arbiser, Jack L.</creator><creator>Hong, Chein-Hui</creator><creator>Govindarajan, Baskaran</creator><creator>Chai, Chih-Yin</creator><creator>Shan, Wan-Ju</creator><creator>Lin, Yu-Fen</creator><creator>Chen, Gwo-Shing</creator><creator>Lee, Chih-Hung</creator><general>Blackwell Publishing Ltd</general><scope>BSCLL</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>7X8</scope></search><sort><creationdate>201008</creationdate><title>Enhanced MCP-1 release by keloid CD14+ cells augments fibroblast proliferation: role of MCP-1 and Akt pathway in keloids</title><author>Liao, Wei-Ting ; 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Experimental Dermatology 2010; 19: e142–e150. :  Keloids are fibrous overgrowth induced by cutaneous injury. The pathogenesis of keloids is poorly understood, and no convincing animal model exists. Current hypotheses of the pathogenesis classify keloids as an entity of aberrant fibrosis. Hyperactivation of the MCP‐1/CCR2 axis reportedly causes fibrosis in liver cirrhosis, atherosclerosis and lung fibrosis. Circulating CD14+ monocytes are precursors of circulating fibrocytes and contribute to fibrogenesis by a MCP‐1/CCR2‐dependent loop. As there is an increase in monocyte lineages in keloids, the aim of this study is to determine whether peripheral CD14+ monocytes in keloid patients trigger fibroblast proliferation through MCP‐1. Expressions of MCP‐1 and its receptor CCR2 in keloid lesions were measured by immunohistochemistry and real‐time PCR. The results revealed an increase in MCP‐1 and CCR2 in the keloid tissues. Co‐culture of keloid CD14+ cells and normal fibroblasts enhanced fibroblast proliferation and a parallel increase in extracellular MCP‐1. We further found that MCP‐1 modest enhanced fibroblast proliferation via Akt activation. Blockade of either MCP‐1 or Akt signaling suppressed the mediation of fibroblast proliferation by CD14+ cells from patients. These results demonstrated that enhanced MCP‐1 release by keloid CD14+ cells augments fibroblast proliferation via Akt pathway in keloids. We concluded that enhanced MCP‐1 release by keloid CD14+ cells augments fibroblast proliferation, which might initiate keloid development.</abstract><cop>Oxford, UK</cop><pub>Blackwell Publishing Ltd</pub><pmid>20100200</pmid><doi>10.1111/j.1600-0625.2009.01021.x</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record>
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ispartof Experimental dermatology, 2010-08, Vol.19 (8), p.e142-e150
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subjects Adolescent
Adult
Akt
Case-Control Studies
Cell Proliferation
Cells, Cultured
Chemokine CCL2 - metabolism
Coculture Techniques
Female
fibroblast proliferation
Fibroblasts - pathology
Humans
keloid
Keloid - metabolism
Lipopolysaccharide Receptors - metabolism
Male
MCP-1
Monocytes - immunology
Monocytes - pathology
monocytes/macrophages
Proto-Oncogene Proteins c-akt - metabolism
Receptors, CCR2 - metabolism
Signal Transduction - physiology
Young Adult
title Enhanced MCP-1 release by keloid CD14+ cells augments fibroblast proliferation: role of MCP-1 and Akt pathway in keloids
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