TY - JOUR
T1 - Overexpression of connective tissue growth factor in podocytes worsens diabetic nephropathy in mice
AU - Yokoi, H.
AU - Mukoyama, M.
AU - Mori, K.
AU - Kasahara, M.
AU - Suganami, T.
AU - Sawai, K.
AU - Yoshioka, T.
AU - Saito, Y.
AU - Ogawa, Y.
AU - Kuwabara, T.
AU - Sugawara, A.
AU - Nakao, K.
N1 - Funding Information:
This work was supported in part by research grants from the Japanese Ministry of Education, Culture, Sports, Science and Technology; the Japanese Ministry of Health, Labour and Welfare; Astellas Foundation for Research on Metabolic Disorders; Smoking Research Foundation; and the Salt Science Research Foundation. We gratefully acknowledge Dr N Oliver and Dr QJ Wang (FibroGen Inc.) for providing anti-CTGF antibody and for valuable discussion, and Dr J Miyazaki (Osaka University, Japan) for providing the transgene vector. We also gratefully acknowledge Mr M Fujimoto, Ms J Nakamura, M Yamada, Mr Y Sakashita, Ms Y Ogawa, and Mr S Nishii for technical assistance, and Ms S Doi, Ms A Sonoda, and Ms A Yamamoto for secretarial assistance.
PY - 2008/2
Y1 - 2008/2
N2 - Connective tissue growth factor (CTGF) is a potent inducer of extracellular matrix accumulation. In diabetic nephropathy, CTGF expression is markedly upregulated both in podocytes and mesangial cells, and this may play an important role in its pathogenesis. We established podocyte-specific CTGF-transgenic mice, which were indistinguishable at baseline from their wild-type littermates. Twelve weeks after streptozotocin-induced diabetes, these transgenic mice showed a more severe proteinuria, mesangial expansion, and a decrease in matrix metalloproteinase-2 activity compared to diabetic wild-type mice. Furthermore, diabetic transgenic mice exhibited less podocin expression and a decreased number of diffusely vacuolated podocytes compared to diabetic wild-type mice. Importantly, induction of diabetes in CTGF-transgenic mice resulted in a further elevation of endogenous CTGF mRNA expression and protein in the glomerular mesangium. Our findings suggest that overexpression of CTGF in podocytes is sufficient to exacerbate proteinuria and mesangial expansion through a functional impairment and loss of podocytes.
AB - Connective tissue growth factor (CTGF) is a potent inducer of extracellular matrix accumulation. In diabetic nephropathy, CTGF expression is markedly upregulated both in podocytes and mesangial cells, and this may play an important role in its pathogenesis. We established podocyte-specific CTGF-transgenic mice, which were indistinguishable at baseline from their wild-type littermates. Twelve weeks after streptozotocin-induced diabetes, these transgenic mice showed a more severe proteinuria, mesangial expansion, and a decrease in matrix metalloproteinase-2 activity compared to diabetic wild-type mice. Furthermore, diabetic transgenic mice exhibited less podocin expression and a decreased number of diffusely vacuolated podocytes compared to diabetic wild-type mice. Importantly, induction of diabetes in CTGF-transgenic mice resulted in a further elevation of endogenous CTGF mRNA expression and protein in the glomerular mesangium. Our findings suggest that overexpression of CTGF in podocytes is sufficient to exacerbate proteinuria and mesangial expansion through a functional impairment and loss of podocytes.
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U2 - 10.1038/sj.ki.5002722
DO - 10.1038/sj.ki.5002722
M3 - Article
C2 - 18075496
AN - SCOPUS:38749131227
SN - 0085-2538
VL - 73
SP - 446
EP - 455
JO - Kidney International
JF - Kidney International
IS - 4
ER -