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and CTGF have overlapping and distinct fibrogenic
effects on human renal cells
Divisions of 1 Rheumatology and Immunology and 3 Nephrology, 2 Department of Pathology and Laboratory Medicine, Medical University of South Carolina, Charleston, South Carolina 29425; and 4 Department of Cell Biology and Anatomy, University of Miami School of Medicine, Miami, Florida 33136
Transforming growth factor-
(TGF-) and connective tissue growth factor (CTGF) are ubiquitously
expressed in various forms of tissue fibrosis, including fibrotic
diseases of the kidney. To clarify the common and divergent roles
of these growth factors in the cells responsible for pathological
extracellular matrix (ECM) deposition in renal fibrosis, the effects of
TGF- and CTGF on ECM expression in primary human mesangial (HMCs)
and human proximal tubule epithelial cells (HTECs) were studied. Both
TGF- and CTGF significantly induced collagen protein expression with similar potency in HMCs. Additionally, 
2(I)-collagen
promoter activity and mRNA levels were similarly induced by TGF- and
CTGF in HMCs. However, only TGF- stimulated collagenous protein
synthesis in HTECs. HTEC expression of tenascin-C (TN-C) was increased
by TGF- and CTGF, although TGF- was the more potent inducer. Thus both growth factors elicit similar profibrogenic effects on ECM production in HMCs, while promoting divergent effects in HTECs. CTGF
induction of TN-C, a marker of epithelial-mesenchymal
transdifferentiation (EMT), with no significant induction of
collagenous protein synthesis in HTECs, may suggest a more predominant
role for CTGF in EMT rather than induction of excessive collagen
deposition by HTECs during renal fibrosis.
mesangial cells; tubule epithelial cells; collagen; tenascin; epithelial-mesenchymal transdifferentiation; connective tissue growth
factor; transforming growth factor-
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