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Mechanism of inhibition on L929 rat fibroblasts proliferation induced by potential adhesion barrier material poly(p‐dioxanone‐co‐ l ‐phenylalanine) electrospun membranes
Author(s) -
Wang Bing,
Dong Jun,
Li Qijie,
Xiong Zuochun,
Xiong Chengdong,
Chen Dongliang
Publication year - 2014
Publication title -
journal of biomedical materials research part a
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.849
H-Index - 150
eISSN - 1552-4965
pISSN - 1549-3296
DOI - 10.1002/jbm.a.35077
Subject(s) - apoptosis , adhesion , fibroblast , phenylalanine , cell adhesion , materials science , membrane , cell growth , microbiology and biotechnology , biochemistry , in vitro , chemistry , biology , amino acid , composite material
Fibroblast plays an important role in the occurrence of postoperative tissue adhesion; materials that have particular “cell–material” interactions to inhibit proliferation of fibroblast will be excellent potential adhesion barriers. In the current study, we synthesized copolymers of p‐dioxanone and l ‐phenylalanine (PDPA) and evaluated the mechanism of its particular inhibition effect on L929 fibroblast proliferation when used as a culture surface. PDPA electrospun membranes could induce apoptosis of L929 fibroblasts. We hypothesized there were two reasons for the apoptosis induction: one was the ability to facilitate cell adhesion of materials, and the other was production of the degradation product, l ‐phenylalanine. Ninhydrin colorimetric results revealed that l ‐phenylalanine was continuously released during the culture process and could induce apoptosis in L929 cells. Relatively poor cell adhesion and constant release of l ‐phenylalanine made PDPA‐1 to be the most efficient polymer for the induction of apoptosis. Analysis of apoptosis‐related genes revealed that PDPA‐induced apoptosis might be performed in a mitochondrial‐dependent pathway. But poly(p‐dioxanone)‐induced apoptosis might occur in a c‐Myc independent pathway that was different from PDPA. © 2014 Wiley Periodicals, Inc. J Biomed Mater Res Part A: 102A: 4062–4070, 2014.