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Am J Physiol Renal Physiol (May 14, 2002). doi:10.1152/ajprenal.00007.2002
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Articles in PresS, published online ahead of print May 14, 2002
Am J Physiol Renal Physiol, 10.1152/ajprenal.00007.2002
Submitted on January 7, 2002
Accepted on May 6, 2002

TGF-ß and CTGF have overlapping and distinct fibrogenic effects on human renal cells

Elizabeth Gore Hyer1, Daniel Shegogue1, Malgorzata Markiewicz1, Shianlen Lo1, Debra Hazen-Martin2, Eddie Greene3, Gary Grotendorst4, and Maria Trojanowska1*

1 Division of Rheumatology & Immunology, Medical University of South Carolina, Charleston, SC, USA
2 Department of Pathology & Laboratory Medicine, Medical University of South Carolina, Charleston, SC, USA
3 Division of Nephrology, Medical University of South Carolina, Charleston, SC, USA; Department of Internal Medicine, Nephrology Division, Mayo Clinic, Rochester, MN, USA
4 Department of Cell Biology & Anatomy, University of Miami School of Medicine, Miami, FL, USA

* To whom correspondence should be addressed. E-mail: trojanme{at}musc.edu.

TGF-ß and 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 pathologic extracellular matrix (ECM) deposition in renal fibrosis, the effects of TGF-ß and CTGF on ECM expression in primary human mesangial (HMCs) and human proximal tubule epithelial (HTECs) cells were studied. Both TGF-ß and CTGF significantly induced collagen protein expression with similar potency in HMCs. Additionally, collagen{alpha}2(I) promoter activity and mRNA levels were similarly induced by TGF-ß and CTGF. However, only TGF-ß stimulated collagenous protein synthesis in HTECs. HTEC expression of tenascin-C (TN-C) was increased by TGF-ß and CTGF, although TGF-ß 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.




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