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Department of Medicine and Clinical Science, Kyoto University Graduate School of Medicine, Kyoto 606-8507, Japan
Connective tissue growth
factor (CTGF) is one of the candidate factors mediating downstream
events of transforming growth factor-
(TGF-), but its role
in fibrogenic properties of TGF- and in tubulointerstitial fibrosis
has not yet been clarified. Using unilateral ureteral obstruction (UUO)
in rats, we analyzed gene expression of TGF-1, CTGF, and
fibronectin. We further investigated the effect of blockade of
endogenous CTGF on TGF--induced fibronectin expression in cultured
rat renal fibroblasts by antisense oligodeoxynucleotide (ODN)
treatment. After UUO, CTGF mRNA expression in the obstructed kidney was significantly upregulated subsequent to TGF-1, followed by marked induction of fibronectin mRNA. By in situ hybridization, CTGF
mRNA was detected mainly in the interstitial fibrotic areas and tubular
epithelial cells as well as in parietal glomerular epithelial cells in
the obstructed kidney. The interstitial cells expressing CTGF mRNA were
also positive for 
-smooth muscle actin. CTGF antisense ODN
transfected into cultured renal fibroblasts significantly attenuated
TGF--stimulated upregulation of fibronectin mRNA and protein
compared with control ODN transfection, together with inhibited
synthesis of type I collagen. With the use of a reporter assay, rat
fibronectin promoter activity was increased by 2.5-fold with
stimulation by TGF-1, and this increase was abolished with antisense
CTGF treatment. Thus CTGF plays a crucial role in fibronectin synthesis
induced by TGF-, suggesting that CTGF blockade could be a possible
therapeutic target against tubulointerstitial fibrosis.
transforming growth factor-; in situ hybridization; obstructive
nephropathy; antisense oligonucleotide; reporter assay
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