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McClellanville Library
9 a.m. - 6 p.m.
Phone: (843) 887-3699
Folly Beach Library
Closed
Phone: (843) 588-2001
Miss Jane's Building (Edisto Library Temporary Location)
2 p.m. – 6 p.m.
Phone: (843) 869-2355
Main Library
9 a.m. - 8 p.m.
Phone: (843) 805-6930
West Ashley Library
9 a.m. - 7 p.m.
Phone: (843) 766-6635
John L. Dart Library
9 a.m. - 7 p.m.
Phone: (843) 722-7550
St. Paul's/Hollywood Library
9 a.m. - 8 p.m.
Phone: (843) 889-3300
Mt. Pleasant Library
9 a.m. – 8 p.m.
Phone: (843) 849-6161
Dorchester Road Library
9 a.m. - 8 p.m.
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Edgar Allan Poe/Sullivan's Island Library
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John's Island Library
9 a.m. - 8 p.m.
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Wando Mount Pleasant Library
9 a.m. - 8 p.m.
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Otranto Road Library
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Hurd/St. Andrews Library
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Baxter-Patrick James Island
9 a.m. - 8 p.m.
Phone: (843) 795-6679
Bees Ferry West Ashley Library
9 a.m. - 8 p.m.
Phone: (843) 805-6892
Village Library
9 a.m. - 1 p.m.
Phone: (843) 884-9741
Keith Summey North Charleston Library
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Phone: (843) 744-2489
Mobile Library
9 a.m. - 5 p.m.
Phone: (843) 805-6909
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TGF-β Isoform Specific Regulation of Airway Inflammation and Remodelling in a Murine Model of Asthma.
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- Author(s): Bottoms, Stephen E.1; Howell, Jane E.1; Reinhardt, Alistair K.1; Evans, Iona C.1; McAnulty, Robin J.1
- Source:
PLoS ONE. 2010, Vol. 5 Issue 3, p1-11. 11p.- Subject Terms:
- Source:
- Additional Information
- Abstract: The TGF-β family of mediators are thought to play important roles in the regulation of inflammation and airway remodelling in asthma. All three mammalian isoforms of TGF-β, TGF-β1-3, are expressed in the airways and TGF-β1 and -β2 are increased in asthma. However, there is little information on the specific roles of individual TGF-β isoforms. In this study we assess the roles of TGF-β1 and TGF-β2 in the regulation of allergen-induced airway inflammation and remodelling associated with asthma, using a validated murine model of ovalbumin sensitization and challenge, and isoform specific TGF-β neutralising antibodies. Antibodies to both isoforms inhibited TGF-β mediated Smad signalling. Anti-TGF-β1 and anti-TGF-β2 inhibited ovalbumin-induced sub-epithelial collagen deposition but anti-TGF-β1 also specifically regulated airway and fibroblast decorin deposition by TGF-β1. Neither antibody affected the allergen-induced increase in sub-epithelial fibroblast-like cells. Anti- TGF-β1 also specifically inhibited ovalbumin-induced increases in monocyte/macrophage recruitment. Whereas, both TGF-β1 and TGF-β2 were involved in regulating allergen-induced increases in eosinophil and lymphocyte numbers. These data show that TGF-β1 and TGF-β2 exhibit a combination of specific and shared roles in the regulation of allergen-induced airway inflammation and remodelling. They also provide evidence in support of the potential for therapeutic regulation of specific subsets of cells and extracellular matrix proteins associated with inflammation and remodelling in airway diseases such as asthma and COPD, as well as other fibroproliferative diseases. [ABSTRACT FROM AUTHOR]
- Abstract: Copyright of PLoS ONE is the property of Public Library of Science and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)
- Abstract:
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