2006Acta Universitatis Medicinalis NanjingRequires access

Effects of endogenous connective tissue growth factor on renal tubular epithelial- myofibroblast transdifferentiation regulated by transforming growth faltor β_1 in vitro

XU Song-zhou

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Abstract

Objective: To investigate the significance of endogenous connective tissue growth factor (CTGF) in epithel ial- myofibroblast transdifferentiation of human renal tubular epithelial cell line(HK2) in vitro. Methods: Cultured HK2 were divided into four groups: (1)control; (2)treated with TGF-β1(5 ng/ml); (3)treated with TGF-β1(5 ng/ml) plus CTGF antisense oligonucleotide (3 mmol/L) ; (4)treated with TGF-β1(5 ng/ml) plus CTGF sense oligonucleotide (3 mmol/L). The cell morphological changes were traced with inverted microscope, and the expression of CTGF、E-cadherin、α-smooth muscle actin (α-SMA) and fibronectin(FN) mRNAs were detected by RT-PCR. Results: In HK2 cells, TGF-β1 stimulated the oval-to-fusiform transdifferentiation in morphology, downregulated E-cadherin mRNA expression, upregulated CTGF, α-SMA and FN mRNAs expression. The presence of the change of CTGF mRNA expression preceded those of E-cadherin、α-SMA and FN mRNAs; CTGF antisense oligonucleotide inhibited these effects by TGF-β1. Conclusion: Endogenous CTGF mediates the regulation of transforming growth factor β1 in human renal tubular epithelial-myofibroblast transdifferentiation in vitro.

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Objective: To investigate the significance of endogenous connective tissue growth factor (CTGF) in epithel ial- myofibroblast transdifferentiation of human renal tubular epithelial cell line(HK2) in vitro. Methods: Cultured HK2 were divided into four groups: (1)control; (2)treated with TGF-β1(5 ng/ml); (3)treated with TGF-β1(5 ng/ml) plus CTGF antisense oligonucleotide (3 mmol/L) ; (4)treated with TGF-β1(5 ng/ml) plus CTGF sense oligonucleotide (3 mmol/L). The cell morphological changes were traced with inverted microscope, and the expression of CTGF、E-cadherin、α-smooth muscle actin (α-SMA) and fibronectin(FN) mRNAs were detected by RT-PCR. Results: In HK2 cells, TGF-β1 stimulated the oval-to-fusiform transdifferentiation in morphology, downregulated E-cadherin mRNA expression, upregulated CTGF, α-SMA and FN mRNAs expression. The presence of the change of CTGF mRNA expression preceded those of E-cadherin、α-SMA and FN mRNAs; CTGF antisense oligonucleotide inhibited these effects by TGF-β1. Conclusion: Endogenous CTGF mediates the regulation of transforming growth factor β1 in human renal tubular epithelial-myofibroblast transdifferentiation in vitro.

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Available abstract

Objective: To investigate the significance of endogenous connective tissue growth factor (CTGF) in epithel ial- myofibroblast transdifferentiation of human renal tubular epithelial cell line(HK2) in vitro. Methods: Cultured HK2 were divided into four groups: (1)control; (2)treated with TGF-β1(5 ng/ml); (3)treated with TGF-β1(5 ng/ml) plus CTGF antisense oligonucleotide (3 mmol/L) ; (4)treated with TGF-β1(5 ng/ml) plus CTGF sense oligonucleotide (3 mmol/L). The cell morphological changes were traced with inverted microscope, and the expression of CTGF、E-cadherin、α-smooth muscle actin (α-SMA) and fibronectin(FN) mRNAs were detected by RT-PCR. Results: In HK2 cells, TGF-β1 stimulated the oval-to-fusiform transdifferentiation in morphology, downregulated E-cadherin mRNA expression, upregulated CTGF, α-SMA and FN mRNAs expression. The presence of the change of CTGF mRNA expression preceded those of E-cadherin、α-SMA and FN mRNAs; CTGF antisense oligonucleotide inhibited these effects by TGF-β1. Conclusion: Endogenous CTGF mediates the regulation of transforming growth factor β1 in human renal tubular epithelial-myofibroblast transdifferentiation in vitro.

Key concepts: CTGF, Transdifferentiation, Myofibroblast, Growth factor, Connective tissue, Transforming growth factor, Biology, Fibronectin

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