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Characterization and regulation of the latent transforming growth factor‐β complex secreted by vascular pericytes
Author(s) -
Marra Fabio,
Bonewald Lynda F.,
ParkSnyder Shaun,
Park InSeok,
Woodruff Kathleen A.,
Abboud Hanna E.
Publication year - 1996
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/(sici)1097-4652(199603)166:3<537::aid-jcp8>3.0.co;2-q
Subject(s) - transforming growth factor , secretion , growth factor , biology , tgf alpha , epidermal growth factor , kidney , extracellular matrix , medicine , endocrinology , microbiology and biotechnology , chemistry , biochemistry , receptor
Transforming growth factor‐β (TGF‐β) stimulates the accumulation of extracellular matrix in renal and hepatic disease. Kidney glomerular mesangial cells (GMC) and liver fat‐storing cells (FSC) produce latent or inactive TGF‐β. In this study, we characterized the latent TGF‐β complexes secreted by these cells. Human FSC produce a single latent TGF‐β complex, predominantly of the TGF‐β1 isoform, whereas GMC secrete multiple complexes of latent TGF‐β, containing β1 and β2 isoforms. At least four forms were identified in GMC using ion exchange chromatography, including a peak not previously described in other cell types which eluted at 0.12 M NaCl, and predominantly of the β2 isoform. Both cell types secrete the latent TGF‐β1 binding protein of 190 kDa, as part of a high molecular weight TGF‐β complex. Epidermal growth factor stimulates the secretion of latent TGF‐β and latent TGF‐β binding protein in both cell types. Secretion of the latent TGF‐β in both cell types was found to be associated with secretion of decorin. This study shows that vascular pericytes from the kidney and the liver have distinctly different profiles of latent TGF‐β complexes, with GMC secreting a unique form of latent TGF‐β2. The regulatory effect of epidermal growth factor and platelet‐derived growth factor has potential implication for the pathophysiology of liver regeneration and chronic liver and kidney diseases. © 1996 Wiley‐Liss, Inc.