Expression and Role of the Hyaluronan Receptor RHAMM in Inflammation after Bleomycin Injury
Lung injury is associated with increased concentrations of hyaluronan (hyaluronic acid, HA). HA modifies cell behavior through interaction with cell-associated receptors such as receptor for HA-mediated motility (RHAMM, CD168). Using a function blocking anti-RHAMM antibody (R36), we investigated the...
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| Veröffentlicht in: | American journal of respiratory cell and molecular biology 2005-11, Vol.33 (5), p.447-454 |
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| creator | Zaman, Aisha Cui, Zheng Foley, Joseph P Zhao, Hengjiang Grimm, Paul C DeLisser, Horace M Savani, Rashmin C |
| description | Lung injury is associated with increased concentrations of hyaluronan (hyaluronic acid, HA). HA modifies cell behavior through interaction with cell-associated receptors such as receptor for HA-mediated motility (RHAMM, CD168). Using a function blocking anti-RHAMM antibody (R36), we investigated the expression and role of RHAMM in the inflammatory response to intratracheal bleomycin in rats. Immunostaining showed increased expression of RHAMM in macrophages 4-7 d after injury. Surface biotin labeling of cells isolated by lavage confirmed increased surface expression of a 70-kD RHAMM after lung injury, and in situ hybridization demonstrated increased RHAMM mRNA in macrophages responding to injury. Time-lapse cinemicrography demonstrated a 5-fold increase in motility of alveolar macrophages from bleomycin-treated animals that was completely blocked by R36 in vitro. Further, HA-stimulated macrophage chemotaxis was also inhibited by R36. Daily administration of R36 to injured animals resulted in a 40% decrease in macrophage accumulation 7 d after injury. Further, H&E staining of tissue sections showed that bleomycin-mediated changes in lung architecture were improved with R36 treatment. Taken together with previous results showing the inhibitory effects of HA-binding peptide on inflammation and fibrosis, we conclude that the interaction of RHAMM with HA is a critical component of the recruitment of inflammatory cells to the lung after injury. |
| doi_str_mv | 10.1165/rcmb.2004-0333OC |
| format | Article |
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HA modifies cell behavior through interaction with cell-associated receptors such as receptor for HA-mediated motility (RHAMM, CD168). Using a function blocking anti-RHAMM antibody (R36), we investigated the expression and role of RHAMM in the inflammatory response to intratracheal bleomycin in rats. Immunostaining showed increased expression of RHAMM in macrophages 4-7 d after injury. Surface biotin labeling of cells isolated by lavage confirmed increased surface expression of a 70-kD RHAMM after lung injury, and in situ hybridization demonstrated increased RHAMM mRNA in macrophages responding to injury. Time-lapse cinemicrography demonstrated a 5-fold increase in motility of alveolar macrophages from bleomycin-treated animals that was completely blocked by R36 in vitro. Further, HA-stimulated macrophage chemotaxis was also inhibited by R36. Daily administration of R36 to injured animals resulted in a 40% decrease in macrophage accumulation 7 d after injury. Further, H&E staining of tissue sections showed that bleomycin-mediated changes in lung architecture were improved with R36 treatment. Taken together with previous results showing the inhibitory effects of HA-binding peptide on inflammation and fibrosis, we conclude that the interaction of RHAMM with HA is a critical component of the recruitment of inflammatory cells to the lung after injury.</description><identifier>ISSN: 1044-1549</identifier><identifier>EISSN: 1535-4989</identifier><identifier>DOI: 10.1165/rcmb.2004-0333OC</identifier><identifier>PMID: 16037485</identifier><identifier>CODEN: AJRBEL</identifier><language>eng</language><publisher>United States: Am Thoracic Soc</publisher><subject>Animals ; Antibodies, Blocking - pharmacology ; Bleomycin - toxicity ; Cell Membrane - chemistry ; Chemotaxis ; Extracellular Matrix Proteins - analysis ; Extracellular Matrix Proteins - antagonists & inhibitors ; Extracellular Matrix Proteins - metabolism ; Hyaluronan Receptors - analysis ; Hyaluronan Receptors - metabolism ; Hyaluronic Acid - metabolism ; Hyaluronic Acid - pharmacology ; Lung - drug effects ; Lung - pathology ; Macrophages - chemistry ; Macrophages - immunology ; Macrophages - metabolism ; Male ; Pneumonia - chemically induced ; Pneumonia - immunology ; Rats ; Rats, Sprague-Dawley</subject><ispartof>American journal of respiratory cell and molecular biology, 2005-11, Vol.33 (5), p.447-454</ispartof><rights>Copyright American Thoracic Society Nov 2005</rights><rights>Copyright © 2005, American Thoracic Society</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c501t-c203783eeb51edd6745c40fd0b1a78cc27cc95f23493cf38337f7971145cac063</citedby><cites>FETCH-LOGICAL-c501t-c203783eeb51edd6745c40fd0b1a78cc27cc95f23493cf38337f7971145cac063</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,776,780,881,27901,27902</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/16037485$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Zaman, Aisha</creatorcontrib><creatorcontrib>Cui, Zheng</creatorcontrib><creatorcontrib>Foley, Joseph P</creatorcontrib><creatorcontrib>Zhao, Hengjiang</creatorcontrib><creatorcontrib>Grimm, Paul C</creatorcontrib><creatorcontrib>DeLisser, Horace M</creatorcontrib><creatorcontrib>Savani, Rashmin C</creatorcontrib><title>Expression and Role of the Hyaluronan Receptor RHAMM in Inflammation after Bleomycin Injury</title><title>American journal of respiratory cell and molecular biology</title><addtitle>Am J Respir Cell Mol Biol</addtitle><description>Lung injury is associated with increased concentrations of hyaluronan (hyaluronic acid, HA). HA modifies cell behavior through interaction with cell-associated receptors such as receptor for HA-mediated motility (RHAMM, CD168). Using a function blocking anti-RHAMM antibody (R36), we investigated the expression and role of RHAMM in the inflammatory response to intratracheal bleomycin in rats. Immunostaining showed increased expression of RHAMM in macrophages 4-7 d after injury. Surface biotin labeling of cells isolated by lavage confirmed increased surface expression of a 70-kD RHAMM after lung injury, and in situ hybridization demonstrated increased RHAMM mRNA in macrophages responding to injury. Time-lapse cinemicrography demonstrated a 5-fold increase in motility of alveolar macrophages from bleomycin-treated animals that was completely blocked by R36 in vitro. Further, HA-stimulated macrophage chemotaxis was also inhibited by R36. Daily administration of R36 to injured animals resulted in a 40% decrease in macrophage accumulation 7 d after injury. Further, H&E staining of tissue sections showed that bleomycin-mediated changes in lung architecture were improved with R36 treatment. 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HA modifies cell behavior through interaction with cell-associated receptors such as receptor for HA-mediated motility (RHAMM, CD168). Using a function blocking anti-RHAMM antibody (R36), we investigated the expression and role of RHAMM in the inflammatory response to intratracheal bleomycin in rats. Immunostaining showed increased expression of RHAMM in macrophages 4-7 d after injury. Surface biotin labeling of cells isolated by lavage confirmed increased surface expression of a 70-kD RHAMM after lung injury, and in situ hybridization demonstrated increased RHAMM mRNA in macrophages responding to injury. Time-lapse cinemicrography demonstrated a 5-fold increase in motility of alveolar macrophages from bleomycin-treated animals that was completely blocked by R36 in vitro. Further, HA-stimulated macrophage chemotaxis was also inhibited by R36. Daily administration of R36 to injured animals resulted in a 40% decrease in macrophage accumulation 7 d after injury. Further, H&E staining of tissue sections showed that bleomycin-mediated changes in lung architecture were improved with R36 treatment. Taken together with previous results showing the inhibitory effects of HA-binding peptide on inflammation and fibrosis, we conclude that the interaction of RHAMM with HA is a critical component of the recruitment of inflammatory cells to the lung after injury.</abstract><cop>United States</cop><pub>Am Thoracic Soc</pub><pmid>16037485</pmid><doi>10.1165/rcmb.2004-0333OC</doi><tpages>8</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Animals Antibodies, Blocking - pharmacology Bleomycin - toxicity Cell Membrane - chemistry Chemotaxis Extracellular Matrix Proteins - analysis Extracellular Matrix Proteins - antagonists & inhibitors Extracellular Matrix Proteins - metabolism Hyaluronan Receptors - analysis Hyaluronan Receptors - metabolism Hyaluronic Acid - metabolism Hyaluronic Acid - pharmacology Lung - drug effects Lung - pathology Macrophages - chemistry Macrophages - immunology Macrophages - metabolism Male Pneumonia - chemically induced Pneumonia - immunology Rats Rats, Sprague-Dawley |
| title | Expression and Role of the Hyaluronan Receptor RHAMM in Inflammation after Bleomycin Injury |
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