Transforming growth factor beta enhances integrin expression and type IV collagenase secretion in human monocytes. Export

@article{Wahl1993, abstract = {Transforming growth factor beta (TGF-beta), secreted within an inflammatory site or injected locally, induces leukocyte margination, chemotaxis, and accumulation. In addition to its potent direct chemotactic activity, TGF-beta may promote this leukocyte response by influencing cell surface integrin expression. At picomolar concentrations, TGF-beta increases steady-state mRNA levels for both the alpha 5 and the beta 1 chain of the fibronectin receptor in human blood monocytes. This increase in gene expression is reflected by selectively enhanced expression of alpha 5 (CDw49e), beta 1 (CDw29), and also alpha 3 (CDw49c) adhesion molecules on the cell surface. Functionally, TGF-beta promotes, in a dose- and time-dependent fashion, monocyte adhesion to type IV collagen, laminin, and fibronectin. Potentially facilitating the movement of monocytes through the extracellular matrix, TGF-beta triggers transcriptional and posttranscriptional regulation of both the 92-kDa and the 72-kDa gelatinase/type IV collagenase. Thus, TGF-beta may play a pivotal role in the early phases of inflammation and repair through its ability to mediate monocyte adhesion, chemotaxis, and enzymatic digestion of extracellular matrix, whereas in chronic lesions, excess TGF-beta may contribute to persistent leukocyte accumulation.}, address = {Laboratories of Immunology, National Institute of Dental Research, National Institutes of Health, Bethesda, MD 20892.}, author = {Wahl, S. M. and Allen, J. B. and Weeks, B. S. and Wong, H. L. and Klotman, P. E.}, citeulike-article-id = {2462603}, citeulike-linkout-0 = {http://view.ncbi.nlm.nih.gov/pubmed/8506302}, citeulike-linkout-1 = {http://www.hubmed.org/display.cgi?uids=8506302}, day = {15}, issn = {0027-8424}, journal = {Proc Natl Acad Sci U S A}, keywords = {activation, regulation}, month = {May}, number = {10}, pages = {4577--4581}, posted-at = {2008-03-04 00:22:48}, priority = {2}, title = {Transforming growth factor beta enhances integrin expression and type IV collagenase secretion in human monocytes.}, url = {http://view.ncbi.nlm.nih.gov/pubmed/8506302}, volume = {90}, year = {1993} }

TY - JOUR ID - Wahl1993 L3 - citeulike-article-id:2462603 N2 - Transforming growth factor beta (TGF-beta), secreted within an inflammatory site or injected locally, induces leukocyte margination, chemotaxis, and accumulation. In addition to its potent direct chemotactic activity, TGF-beta may promote this leukocyte response by influencing cell surface integrin expression. At picomolar concentrations, TGF-beta increases steady-state mRNA levels for both the alpha 5 and the beta 1 chain of the fibronectin receptor in human blood monocytes. This increase in gene expression is reflected by selectively enhanced expression of alpha 5 (CDw49e), beta 1 (CDw29), and also alpha 3 (CDw49c) adhesion molecules on the cell surface. Functionally, TGF-beta promotes, in a dose- and time-dependent fashion, monocyte adhesion to type IV collagen, laminin, and fibronectin. Potentially facilitating the movement of monocytes through the extracellular matrix, TGF-beta triggers transcriptional and posttranscriptional regulation of both the 92-kDa and the 72-kDa gelatinase/type IV collagenase. Thus, TGF-beta may play a pivotal role in the early phases of inflammation and repair through its ability to mediate monocyte adhesion, chemotaxis, and enzymatic digestion of extracellular matrix, whereas in chronic lesions, excess TGF-beta may contribute to persistent leukocyte accumulation. IS - 10 JF - Proc Natl Acad Sci U S A SN - 0027-8424 AD - Laboratories of Immunology, National Institute of Dental Research, National Institutes of Health, Bethesda, MD 20892. EP - 4581 TI - Transforming growth factor beta enhances integrin expression and type IV collagenase secretion in human monocytes. VL - 90 SP - 4577 KW - activation KW - regulation AU - Wahl, SM AU - Allen, JB AU - Weeks, BS AU - Wong, HL AU - Klotman, PE PY - 1993/05/15/ UR - http://view.ncbi.nlm.nih.gov/pubmed/8506302 ER -