Release of biologically active TGF-beta from airway smooth muscle cells induces autocrine synthesis of collagen
In severe or chronic asthma, there is an increase in airway smooth muscle cell (ASMC) mass as well as an increase in connective tissue proteins in the smooth muscle layer of airways. Transforming growth factor-beta (TGF-beta) exists in three isoforms in mammals and is a potent regulator of connectiv...
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| Veröffentlicht in: | American journal of physiology. Lung cellular and molecular physiology 2001-05, Vol.280 (5), p.L999-L1008 |
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| container_end_page | L1008 |
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| container_issue | 5 |
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| container_title | American journal of physiology. Lung cellular and molecular physiology |
| container_volume | 280 |
| creator | Coutts, A Chen, G Stephens, N Hirst, S Douglas, D Eichholtz, T Khalil, N |
| description | In severe or chronic asthma, there is an increase in airway smooth muscle cell (ASMC) mass as well as an increase in connective tissue proteins in the smooth muscle layer of airways. Transforming growth factor-beta (TGF-beta) exists in three isoforms in mammals and is a potent regulator of connective tissue protein synthesis. Using immunohistochemistry, we had previously demonstrated that ASMCs contain large quantities of TGF-beta1-3. In this study, we demonstrate that bovine ASMC-derived TGF-beta associates with the TGF-beta latency binding protein-1 (LTBP-1) expressed by the same cells. The TGF-beta associated with LTBP-1 localizes TGF-beta extracellularly. Furthermore, plasmin, a serine protease, regulates the secretion of a biologically active form of TGF-beta by ASMCs as well as the release of extracellular TGF-beta. The biologically active TGF-beta released by plasmin induces ASMCs to synthesize collagen I in an autocrine manner. The autocrine induction of collagen expression by ASMCs may contribute to the irreversible fibrosis and remodeling seen in the airways of some asthmatics. |
| doi_str_mv | 10.1152/ajplung.2001.280.5.l999 |
| format | Article |
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Transforming growth factor-beta (TGF-beta) exists in three isoforms in mammals and is a potent regulator of connective tissue protein synthesis. Using immunohistochemistry, we had previously demonstrated that ASMCs contain large quantities of TGF-beta1-3. In this study, we demonstrate that bovine ASMC-derived TGF-beta associates with the TGF-beta latency binding protein-1 (LTBP-1) expressed by the same cells. The TGF-beta associated with LTBP-1 localizes TGF-beta extracellularly. Furthermore, plasmin, a serine protease, regulates the secretion of a biologically active form of TGF-beta by ASMCs as well as the release of extracellular TGF-beta. The biologically active TGF-beta released by plasmin induces ASMCs to synthesize collagen I in an autocrine manner. The autocrine induction of collagen expression by ASMCs may contribute to the irreversible fibrosis and remodeling seen in the airways of some asthmatics.</description><identifier>ISSN: 1040-0605</identifier><identifier>EISSN: 1522-1504</identifier><identifier>DOI: 10.1152/ajplung.2001.280.5.l999</identifier><identifier>PMID: 11290525</identifier><language>eng</language><publisher>United States</publisher><subject>Animals ; Aprotinin - pharmacology ; Asthma - complications ; Asthma - metabolism ; Autocrine Communication - physiology ; Biological Assay ; Carrier Proteins - metabolism ; Cattle ; Cells, Cultured ; Collagen - biosynthesis ; Extracellular Space - metabolism ; Fibrinolysin - antagonists & inhibitors ; Fibrinolysin - metabolism ; Fibrinolysin - pharmacology ; Fibrosis - etiology ; Intracellular Signaling Peptides and Proteins ; Latent TGF-beta Binding Proteins ; Mink ; Muscle, Smooth - cytology ; Muscle, Smooth - drug effects ; Muscle, Smooth - metabolism ; Procollagen - biosynthesis ; Serine Proteinase Inhibitors - pharmacology ; Trachea ; Transforming Growth Factor beta - metabolism ; Transforming Growth Factor beta - secretion</subject><ispartof>American journal of physiology. 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Lung cellular and molecular physiology</title><addtitle>Am J Physiol Lung Cell Mol Physiol</addtitle><description>In severe or chronic asthma, there is an increase in airway smooth muscle cell (ASMC) mass as well as an increase in connective tissue proteins in the smooth muscle layer of airways. Transforming growth factor-beta (TGF-beta) exists in three isoforms in mammals and is a potent regulator of connective tissue protein synthesis. Using immunohistochemistry, we had previously demonstrated that ASMCs contain large quantities of TGF-beta1-3. In this study, we demonstrate that bovine ASMC-derived TGF-beta associates with the TGF-beta latency binding protein-1 (LTBP-1) expressed by the same cells. The TGF-beta associated with LTBP-1 localizes TGF-beta extracellularly. Furthermore, plasmin, a serine protease, regulates the secretion of a biologically active form of TGF-beta by ASMCs as well as the release of extracellular TGF-beta. The biologically active TGF-beta released by plasmin induces ASMCs to synthesize collagen I in an autocrine manner. The autocrine induction of collagen expression by ASMCs may contribute to the irreversible fibrosis and remodeling seen in the airways of some asthmatics.</description><subject>Animals</subject><subject>Aprotinin - pharmacology</subject><subject>Asthma - complications</subject><subject>Asthma - metabolism</subject><subject>Autocrine Communication - physiology</subject><subject>Biological Assay</subject><subject>Carrier Proteins - metabolism</subject><subject>Cattle</subject><subject>Cells, Cultured</subject><subject>Collagen - biosynthesis</subject><subject>Extracellular Space - metabolism</subject><subject>Fibrinolysin - antagonists & inhibitors</subject><subject>Fibrinolysin - metabolism</subject><subject>Fibrinolysin - pharmacology</subject><subject>Fibrosis - etiology</subject><subject>Intracellular Signaling Peptides and Proteins</subject><subject>Latent TGF-beta Binding Proteins</subject><subject>Mink</subject><subject>Muscle, Smooth - cytology</subject><subject>Muscle, Smooth - drug effects</subject><subject>Muscle, Smooth - metabolism</subject><subject>Procollagen - biosynthesis</subject><subject>Serine Proteinase Inhibitors - pharmacology</subject><subject>Trachea</subject><subject>Transforming Growth Factor beta - metabolism</subject><subject>Transforming Growth Factor beta - secretion</subject><issn>1040-0605</issn><issn>1522-1504</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2001</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpFkEFrGzEQhUVoaVy3fyHRqbfdjrQryzoWkzgFQ6G4ZzHSztoK2pWz2m3wv8-aGHKagXnvzeNj7F5AKYSSP_H5FKf-UEoAUco1lKqMxpgbtpivshAK6k_zDjUUsAJ1y77m_AwACmD1hd0KIQ0oqRYs_aVImImnlruQYjoEjzGeOfox_Ce-3z4Wjkbk7ZA6jmF4xTPPXUrjkXdT9pG4pxgzD30zecocpzH5IfTE87kfj5RDvmT7FCMeqP_GPrcYM32_ziX79_iw3zwVuz_b35tfu8JXYMaibhpnxLrBtlaNgspho9dIrhbkq2qlQNRCe3JrQVq6RhuFWngnkSo0K1FXS_bjPfc0pJeJ8mi7kC9Nsac0Zas1SK2MmoX6XeiHlPNArT0NocPhbAXYC2t7ZW0vrO3M2iq7m1nPzrvri8l11Hz4rnCrN7x0f3g</recordid><startdate>20010501</startdate><enddate>20010501</enddate><creator>Coutts, A</creator><creator>Chen, G</creator><creator>Stephens, N</creator><creator>Hirst, S</creator><creator>Douglas, D</creator><creator>Eichholtz, T</creator><creator>Khalil, N</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>20010501</creationdate><title>Release of biologically active TGF-beta from airway smooth muscle cells induces autocrine synthesis of collagen</title><author>Coutts, A ; Chen, G ; Stephens, N ; Hirst, S ; Douglas, D ; Eichholtz, T ; Khalil, N</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c309t-4ddb918daf45d503bad78aeb41ec336501417ceb81e72bd795a71cb2ae3a96143</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2001</creationdate><topic>Animals</topic><topic>Aprotinin - pharmacology</topic><topic>Asthma - complications</topic><topic>Asthma - metabolism</topic><topic>Autocrine Communication - physiology</topic><topic>Biological Assay</topic><topic>Carrier Proteins - metabolism</topic><topic>Cattle</topic><topic>Cells, Cultured</topic><topic>Collagen - biosynthesis</topic><topic>Extracellular Space - metabolism</topic><topic>Fibrinolysin - antagonists & inhibitors</topic><topic>Fibrinolysin - metabolism</topic><topic>Fibrinolysin - pharmacology</topic><topic>Fibrosis - etiology</topic><topic>Intracellular Signaling Peptides and Proteins</topic><topic>Latent TGF-beta Binding Proteins</topic><topic>Mink</topic><topic>Muscle, Smooth - cytology</topic><topic>Muscle, Smooth - drug effects</topic><topic>Muscle, Smooth - metabolism</topic><topic>Procollagen - biosynthesis</topic><topic>Serine Proteinase Inhibitors - pharmacology</topic><topic>Trachea</topic><topic>Transforming Growth Factor beta - metabolism</topic><topic>Transforming Growth Factor beta - secretion</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Coutts, A</creatorcontrib><creatorcontrib>Chen, G</creatorcontrib><creatorcontrib>Stephens, N</creatorcontrib><creatorcontrib>Hirst, S</creatorcontrib><creatorcontrib>Douglas, D</creatorcontrib><creatorcontrib>Eichholtz, T</creatorcontrib><creatorcontrib>Khalil, N</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. 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Lung cellular and molecular physiology</jtitle><addtitle>Am J Physiol Lung Cell Mol Physiol</addtitle><date>2001-05-01</date><risdate>2001</risdate><volume>280</volume><issue>5</issue><spage>L999</spage><epage>L1008</epage><pages>L999-L1008</pages><issn>1040-0605</issn><eissn>1522-1504</eissn><abstract>In severe or chronic asthma, there is an increase in airway smooth muscle cell (ASMC) mass as well as an increase in connective tissue proteins in the smooth muscle layer of airways. Transforming growth factor-beta (TGF-beta) exists in three isoforms in mammals and is a potent regulator of connective tissue protein synthesis. Using immunohistochemistry, we had previously demonstrated that ASMCs contain large quantities of TGF-beta1-3. In this study, we demonstrate that bovine ASMC-derived TGF-beta associates with the TGF-beta latency binding protein-1 (LTBP-1) expressed by the same cells. The TGF-beta associated with LTBP-1 localizes TGF-beta extracellularly. Furthermore, plasmin, a serine protease, regulates the secretion of a biologically active form of TGF-beta by ASMCs as well as the release of extracellular TGF-beta. The biologically active TGF-beta released by plasmin induces ASMCs to synthesize collagen I in an autocrine manner. The autocrine induction of collagen expression by ASMCs may contribute to the irreversible fibrosis and remodeling seen in the airways of some asthmatics.</abstract><cop>United States</cop><pmid>11290525</pmid><doi>10.1152/ajplung.2001.280.5.l999</doi></addata></record> |
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| source | MEDLINE; American Physiological Society; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals |
| subjects | Animals Aprotinin - pharmacology Asthma - complications Asthma - metabolism Autocrine Communication - physiology Biological Assay Carrier Proteins - metabolism Cattle Cells, Cultured Collagen - biosynthesis Extracellular Space - metabolism Fibrinolysin - antagonists & inhibitors Fibrinolysin - metabolism Fibrinolysin - pharmacology Fibrosis - etiology Intracellular Signaling Peptides and Proteins Latent TGF-beta Binding Proteins Mink Muscle, Smooth - cytology Muscle, Smooth - drug effects Muscle, Smooth - metabolism Procollagen - biosynthesis Serine Proteinase Inhibitors - pharmacology Trachea Transforming Growth Factor beta - metabolism Transforming Growth Factor beta - secretion |
| title | Release of biologically active TGF-beta from airway smooth muscle cells induces autocrine synthesis of collagen |
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