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[Effect of synthesized polypeptide (P16) on inhibiting cell transdifferentiation and fibrosis induced by connective tissue growth factor].

Key Laboratory of Transplant Engineering and Immunology, Ministry Of Health, West China Hospital, Sichuan University, Chengdu 610041, China.
Sichuan da xue xue bao. Yi xue ban = Journal of Sichuan University. Medical science edition 08/2007; 38(4):590-4.
Source: PubMed

ABSTRACT To explore the possibility of a CTGF originated hexadeca-peptide (named P16) to compete with the CTGF in binding integrin avP3 on rat tubular epithelial cells (NRK-52E) and inhibit the transdifferentiation and myofibroblasts of NRK-52E cells induced by CTGF.
The NRK-52E cells were cultured in a condition with the existence of CTGF, P16-FITC (P16 labeled with fluorescein isothiocyanate), or both for 24h. The immunofluorescence staining and RT-PCR were employed to detect the expressions of the protein and mRNA of alpha-SMA and the collagen I and IV which indicate the cell trans-differentiation and fibrosis.
The P16 had stronger affinity with the NRK-52E cells than the CTGF. In a CTGF and P16 co-culture system, the P16 inhibited the expression of a-SMA, collagen I and IV up-regulated by the CTGF. However, P16 alone had no effect on cell trans-differentiation and fibrosis.
The synthesized P16 is capable of binding with NRK-52E cells and inhibiting trans-differentiation and fibrosis of the NRK-52E cells induced by CTGF in vitro. This finding offers a possibility of developing a novel antifibrosis therapy that targets CTGF receptor.

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