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MCP-1 in pleural injury: CCR2 mediates haptotaxis of pleural mesothelial cells
Division of Pulmonary and Critical Care Medicine, Veterans Affairs Medical Center, Indiana University School of Medicine, Indianapolis, Indiana 46202 Pleural injury results in the death of mesothelial cells and denudation of the mesothelial basement membrane. Repair of the mesothelium without fibros...
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Published in: | American journal of physiology. Lung cellular and molecular physiology 2000-03, Vol.278 (3), p.591-L598 |
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container_end_page | L598 |
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container_title | American journal of physiology. Lung cellular and molecular physiology |
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creator | Nasreen, Najmunnisa Mohammed, Kamal A Galffy, Gabriella Ward, Melissa J Antony, Veena B |
description | Division of Pulmonary and Critical Care Medicine, Veterans Affairs
Medical Center, Indiana University School of Medicine, Indianapolis,
Indiana 46202
Pleural injury results
in the death of mesothelial cells and denudation of the mesothelial
basement membrane. Repair of the mesothelium without fibrosis requires
proliferation and migration of mesothelial cells into the injured area.
We hypothesized that monocyte chemoattractant protein-1 (MCP-1) induces
proliferative and haptotactic responses in pleural mesothelial cells
(PMCs) and that the MCP-1 binding receptor CCR2 mediates
the pleural repair process. We demonstrate that PMCs exhibited
MCP-1-specific immunostaining on injury. MCP-1 induced proliferative
and haptotactic responses in PMCs. PMCs express CCR2 in a
time-dependent manner. Fluorescence-activated cell sorting analysis
demonstrated that interleukin (IL)-2 upregulated CCR2 protein
expression in PMCs, whereas lipopolysaccharide (LPS) downregulated the
response at the initial period compared with that in resting PMCs.
However, the inhibitory potential of LPS was lost after 12 h and showed a similar response at 24 and 48 h. Haptotactic migration was
upregulated in PMCs that were cultured in the presence of IL-2. The
increased haptotactic capacity of mesothelial cells in the presence of
IL-2 correlated with increased CCR2 mRNA expression. PMCs cultured in
the presence of LPS showed decreased haptotactic activity to MCP-1.
Blocking the CCR2 with neutralizing antibodies decreased the
haptotactic response of PMCs to MCP-1. These results suggest that the
haptotactic migration of mesothelial cells in response to MCP-1 are
mediated through CCR2, which may play a crucial role in
reepithelialization of the denuded basement membrane at the site of
pleural injury and may thus contribute to the regeneration of the
mesothelium during the process of pleural repair.
monocyte chemoattractant protein-1; interleukin-2; lipopolysaccharide |
doi_str_mv | 10.1152/ajplung.2000.278.3.l591 |
format | article |
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Medical Center, Indiana University School of Medicine, Indianapolis,
Indiana 46202
Pleural injury results
in the death of mesothelial cells and denudation of the mesothelial
basement membrane. Repair of the mesothelium without fibrosis requires
proliferation and migration of mesothelial cells into the injured area.
We hypothesized that monocyte chemoattractant protein-1 (MCP-1) induces
proliferative and haptotactic responses in pleural mesothelial cells
(PMCs) and that the MCP-1 binding receptor CCR2 mediates
the pleural repair process. We demonstrate that PMCs exhibited
MCP-1-specific immunostaining on injury. MCP-1 induced proliferative
and haptotactic responses in PMCs. PMCs express CCR2 in a
time-dependent manner. Fluorescence-activated cell sorting analysis
demonstrated that interleukin (IL)-2 upregulated CCR2 protein
expression in PMCs, whereas lipopolysaccharide (LPS) downregulated the
response at the initial period compared with that in resting PMCs.
However, the inhibitory potential of LPS was lost after 12 h and showed a similar response at 24 and 48 h. Haptotactic migration was
upregulated in PMCs that were cultured in the presence of IL-2. The
increased haptotactic capacity of mesothelial cells in the presence of
IL-2 correlated with increased CCR2 mRNA expression. PMCs cultured in
the presence of LPS showed decreased haptotactic activity to MCP-1.
Blocking the CCR2 with neutralizing antibodies decreased the
haptotactic response of PMCs to MCP-1. These results suggest that the
haptotactic migration of mesothelial cells in response to MCP-1 are
mediated through CCR2, which may play a crucial role in
reepithelialization of the denuded basement membrane at the site of
pleural injury and may thus contribute to the regeneration of the
mesothelium during the process of pleural repair.
monocyte chemoattractant protein-1; interleukin-2; lipopolysaccharide</description><identifier>ISSN: 1040-0605</identifier><identifier>EISSN: 1522-1504</identifier><identifier>DOI: 10.1152/ajplung.2000.278.3.l591</identifier><identifier>PMID: 10710532</identifier><language>eng</language><publisher>United States</publisher><subject>Cell Division - physiology ; Cell Movement - physiology ; Cells, Cultured ; Chemokine CCL2 - metabolism ; Epithelial Cells - physiology ; Humans ; Interleukin-2 - pharmacology ; Lipopolysaccharides - pharmacology ; Pleura - injuries ; Pleura - metabolism ; Pleura - pathology ; Pleura - physiopathology ; Receptors, CCR2 ; Receptors, Chemokine ; Receptors, Cytokine - genetics ; Receptors, Cytokine - metabolism ; Receptors, Cytokine - physiology ; RNA, Messenger - metabolism ; Wounds and Injuries - metabolism ; Wounds and Injuries - pathology ; Wounds and Injuries - physiopathology</subject><ispartof>American journal of physiology. Lung cellular and molecular physiology, 2000-03, Vol.278 (3), p.591-L598</ispartof><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c463t-e820095454d3669a33854eb1425836065a717cd5d727c75c20f3fcc234db434b3</citedby><cites>FETCH-LOGICAL-c463t-e820095454d3669a33854eb1425836065a717cd5d727c75c20f3fcc234db434b3</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/10710532$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Nasreen, Najmunnisa</creatorcontrib><creatorcontrib>Mohammed, Kamal A</creatorcontrib><creatorcontrib>Galffy, Gabriella</creatorcontrib><creatorcontrib>Ward, Melissa J</creatorcontrib><creatorcontrib>Antony, Veena B</creatorcontrib><title>MCP-1 in pleural injury: CCR2 mediates haptotaxis of pleural mesothelial cells</title><title>American journal of physiology. Lung cellular and molecular physiology</title><addtitle>Am J Physiol Lung Cell Mol Physiol</addtitle><description>Division of Pulmonary and Critical Care Medicine, Veterans Affairs
Medical Center, Indiana University School of Medicine, Indianapolis,
Indiana 46202
Pleural injury results
in the death of mesothelial cells and denudation of the mesothelial
basement membrane. Repair of the mesothelium without fibrosis requires
proliferation and migration of mesothelial cells into the injured area.
We hypothesized that monocyte chemoattractant protein-1 (MCP-1) induces
proliferative and haptotactic responses in pleural mesothelial cells
(PMCs) and that the MCP-1 binding receptor CCR2 mediates
the pleural repair process. We demonstrate that PMCs exhibited
MCP-1-specific immunostaining on injury. MCP-1 induced proliferative
and haptotactic responses in PMCs. PMCs express CCR2 in a
time-dependent manner. Fluorescence-activated cell sorting analysis
demonstrated that interleukin (IL)-2 upregulated CCR2 protein
expression in PMCs, whereas lipopolysaccharide (LPS) downregulated the
response at the initial period compared with that in resting PMCs.
However, the inhibitory potential of LPS was lost after 12 h and showed a similar response at 24 and 48 h. Haptotactic migration was
upregulated in PMCs that were cultured in the presence of IL-2. The
increased haptotactic capacity of mesothelial cells in the presence of
IL-2 correlated with increased CCR2 mRNA expression. PMCs cultured in
the presence of LPS showed decreased haptotactic activity to MCP-1.
Blocking the CCR2 with neutralizing antibodies decreased the
haptotactic response of PMCs to MCP-1. These results suggest that the
haptotactic migration of mesothelial cells in response to MCP-1 are
mediated through CCR2, which may play a crucial role in
reepithelialization of the denuded basement membrane at the site of
pleural injury and may thus contribute to the regeneration of the
mesothelium during the process of pleural repair.
monocyte chemoattractant protein-1; interleukin-2; lipopolysaccharide</description><subject>Cell Division - physiology</subject><subject>Cell Movement - physiology</subject><subject>Cells, Cultured</subject><subject>Chemokine CCL2 - metabolism</subject><subject>Epithelial Cells - physiology</subject><subject>Humans</subject><subject>Interleukin-2 - pharmacology</subject><subject>Lipopolysaccharides - pharmacology</subject><subject>Pleura - injuries</subject><subject>Pleura - metabolism</subject><subject>Pleura - pathology</subject><subject>Pleura - physiopathology</subject><subject>Receptors, CCR2</subject><subject>Receptors, Chemokine</subject><subject>Receptors, Cytokine - genetics</subject><subject>Receptors, Cytokine - metabolism</subject><subject>Receptors, Cytokine - physiology</subject><subject>RNA, Messenger - metabolism</subject><subject>Wounds and Injuries - metabolism</subject><subject>Wounds and Injuries - pathology</subject><subject>Wounds and Injuries - physiopathology</subject><issn>1040-0605</issn><issn>1522-1504</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2000</creationdate><recordtype>article</recordtype><recordid>eNp1kMtOwzAURC0EoqXwC5AVu4TrV9ywQxEFpPIQKmvLTZzGlduEOBHN3-OqhbJh5ZE8M3d0ELrCEGHMyY1a1rZbLyICABER44hGlif4CA39LwkxB3bsNTAIIQY-QGfOLb2XA8SnaIBBYOCUDNHLc_oW4sCsg9rqrlHWy2XX9LdBmr6TYKVzo1rtglLVbdWqjXFBVfx6V9pVbamt8TrT1rpzdFIo6_TF_h2hj8n9LH0Mp68PT-ndNMxYTNtQj_3whDPOchrHiaJ0zJmeY0b4mMYQcyWwyHKeCyIywTMCBS2yjFCWzxllczpC17veuqk-O-1auTJuu0CtddU5KSCJfVfijWJnzJrKuUYXsm7MSjW9xCC3KOUepdyilB6lpHLqUfrk5f5EN_cY_uR27Lwh2RlKsyi_TKNlXfbOVLZa9HLSWTvTm_an_lAs67zw2fD_7O-iw5hvSQ-VgA</recordid><startdate>20000301</startdate><enddate>20000301</enddate><creator>Nasreen, Najmunnisa</creator><creator>Mohammed, Kamal A</creator><creator>Galffy, Gabriella</creator><creator>Ward, Melissa J</creator><creator>Antony, Veena B</creator><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>20000301</creationdate><title>MCP-1 in pleural injury: CCR2 mediates haptotaxis of pleural mesothelial cells</title><author>Nasreen, Najmunnisa ; Mohammed, Kamal A ; Galffy, Gabriella ; Ward, Melissa J ; Antony, Veena B</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c463t-e820095454d3669a33854eb1425836065a717cd5d727c75c20f3fcc234db434b3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2000</creationdate><topic>Cell Division - physiology</topic><topic>Cell Movement - physiology</topic><topic>Cells, Cultured</topic><topic>Chemokine CCL2 - metabolism</topic><topic>Epithelial Cells - physiology</topic><topic>Humans</topic><topic>Interleukin-2 - pharmacology</topic><topic>Lipopolysaccharides - pharmacology</topic><topic>Pleura - injuries</topic><topic>Pleura - metabolism</topic><topic>Pleura - pathology</topic><topic>Pleura - physiopathology</topic><topic>Receptors, CCR2</topic><topic>Receptors, Chemokine</topic><topic>Receptors, Cytokine - genetics</topic><topic>Receptors, Cytokine - metabolism</topic><topic>Receptors, Cytokine - physiology</topic><topic>RNA, Messenger - metabolism</topic><topic>Wounds and Injuries - metabolism</topic><topic>Wounds and Injuries - pathology</topic><topic>Wounds and Injuries - physiopathology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Nasreen, Najmunnisa</creatorcontrib><creatorcontrib>Mohammed, Kamal A</creatorcontrib><creatorcontrib>Galffy, Gabriella</creatorcontrib><creatorcontrib>Ward, Melissa J</creatorcontrib><creatorcontrib>Antony, Veena B</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>American journal of physiology. Lung cellular and molecular physiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Nasreen, Najmunnisa</au><au>Mohammed, Kamal A</au><au>Galffy, Gabriella</au><au>Ward, Melissa J</au><au>Antony, Veena B</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>MCP-1 in pleural injury: CCR2 mediates haptotaxis of pleural mesothelial cells</atitle><jtitle>American journal of physiology. Lung cellular and molecular physiology</jtitle><addtitle>Am J Physiol Lung Cell Mol Physiol</addtitle><date>2000-03-01</date><risdate>2000</risdate><volume>278</volume><issue>3</issue><spage>591</spage><epage>L598</epage><pages>591-L598</pages><issn>1040-0605</issn><eissn>1522-1504</eissn><abstract>Division of Pulmonary and Critical Care Medicine, Veterans Affairs
Medical Center, Indiana University School of Medicine, Indianapolis,
Indiana 46202
Pleural injury results
in the death of mesothelial cells and denudation of the mesothelial
basement membrane. Repair of the mesothelium without fibrosis requires
proliferation and migration of mesothelial cells into the injured area.
We hypothesized that monocyte chemoattractant protein-1 (MCP-1) induces
proliferative and haptotactic responses in pleural mesothelial cells
(PMCs) and that the MCP-1 binding receptor CCR2 mediates
the pleural repair process. We demonstrate that PMCs exhibited
MCP-1-specific immunostaining on injury. MCP-1 induced proliferative
and haptotactic responses in PMCs. PMCs express CCR2 in a
time-dependent manner. Fluorescence-activated cell sorting analysis
demonstrated that interleukin (IL)-2 upregulated CCR2 protein
expression in PMCs, whereas lipopolysaccharide (LPS) downregulated the
response at the initial period compared with that in resting PMCs.
However, the inhibitory potential of LPS was lost after 12 h and showed a similar response at 24 and 48 h. Haptotactic migration was
upregulated in PMCs that were cultured in the presence of IL-2. The
increased haptotactic capacity of mesothelial cells in the presence of
IL-2 correlated with increased CCR2 mRNA expression. PMCs cultured in
the presence of LPS showed decreased haptotactic activity to MCP-1.
Blocking the CCR2 with neutralizing antibodies decreased the
haptotactic response of PMCs to MCP-1. These results suggest that the
haptotactic migration of mesothelial cells in response to MCP-1 are
mediated through CCR2, which may play a crucial role in
reepithelialization of the denuded basement membrane at the site of
pleural injury and may thus contribute to the regeneration of the
mesothelium during the process of pleural repair.
monocyte chemoattractant protein-1; interleukin-2; lipopolysaccharide</abstract><cop>United States</cop><pmid>10710532</pmid><doi>10.1152/ajplung.2000.278.3.l591</doi></addata></record> |
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source | American Physiological Society Free |
subjects | Cell Division - physiology Cell Movement - physiology Cells, Cultured Chemokine CCL2 - metabolism Epithelial Cells - physiology Humans Interleukin-2 - pharmacology Lipopolysaccharides - pharmacology Pleura - injuries Pleura - metabolism Pleura - pathology Pleura - physiopathology Receptors, CCR2 Receptors, Chemokine Receptors, Cytokine - genetics Receptors, Cytokine - metabolism Receptors, Cytokine - physiology RNA, Messenger - metabolism Wounds and Injuries - metabolism Wounds and Injuries - pathology Wounds and Injuries - physiopathology |
title | MCP-1 in pleural injury: CCR2 mediates haptotaxis of pleural mesothelial cells |
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