Mechanism of inhibition on L929 rat fibroblasts proliferation induced by potential adhesion barrier material poly(p‐dioxanone‐co‐l‐phenylalanine) electrospun membranes. Issue 11 (17th January 2014)

• Record Type: Journal Article
• Authors: Wang, Bing; Dong, Jun; Li, Qijie; Xiong, Zuochun; Xiong, Chengdong; Chen, Dongliang
• Is Part Of: Journal of biomedical materials research. Volume 102:Issue 11(2014)
• Page Start: 4062
• Page End: 4070
• Publication Date: 2014-01-17
• Subjects: Biomedical materials -- Periodicals; 610.28
• DOI: 10.1002/jbm.a.35077
• Languages: English
• ISSNs: 1549-3296

Abstract

<abstract abstract-type="main"> <title>Abstract</title> <p>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 <sc>l</sc>‐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, <sc>l</sc>‐phenylalanine. Ninhydrin colorimetric results revealed that <sc>l</sc>‐phenylalanine was continuously released during the culture process and could induce apoptosis in L929 cells. Relatively poor cell adhesion and constant release of <sc>l</sc>‐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.</p> </abstract>