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


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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