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

SM Wahl, JB Allen, BS Weeks… - Proceedings of the …, 1993 - National Acad Sciences
SM Wahl, JB Allen, BS Weeks, HL Wong, PE Klotman
Proceedings of the National Academy of Sciences, 1993National Acad Sciences
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 …
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.
National Acad Sciences