Effects of antisense oligonucleotides on the expression of focal adhesion kinase gene and collagen synthesis in the cultured human fibroblasts of hypertrophic scar.
- Author:
Rui CHEN
1
;
Min-Gang FU
;
Yi LU
;
Lin WANG
;
Ping PING
;
Zhi-Hong FAN
Author Information
- Publication Type:Journal Article
- MeSH: Cells, Cultured; Cicatrix, Hypertrophic; genetics; metabolism; pathology; Collagen; biosynthesis; Fibroblasts; drug effects; metabolism; Focal Adhesion Protein-Tyrosine Kinases; genetics; metabolism; Humans; Oligonucleotides, Antisense; genetics; pharmacology; Transfection
- From: Chinese Journal of Plastic Surgery 2008;24(6):475-477
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo study the role of focal adhesion kinase (FAK) in the pathogenesis of human hypertrophic scar.
METHODSHuman hypertrophic scar fibroblasts (HSFB) were isolated from human hypertrophic scar and cultured in vitro. The cells were then divided into 3 groups as AT group (phosphorothioate FAK ASODN was transfected into the HSFB by liposome), LPC group (liposome only), and LC group (control group, without liposome or ASODN). The FAKmRNA index of HSFB was assessed by polymerase chain reaction method (FQ-PCR). The collagen synthesis of HSFB was assessed by 3H-proline incorporation method.
RESULTSThe FAK mRNA index of HSFB in AT group 48 hours after transfection was significantly lower than that in LPC and LC groups (0.043 +/- 0.030, 0.124 +/- 0.070, 0.127 +/- 0.0195, P < 0.05). The 3H-proline incorporation rate in AT group was lower than that in LPC and LC groups (257.0 +/- 15.14, 962.2 +/- 300.5, 930.8 +/- 28.97, P < 0.01).
CONCLUSIONThe expression of FAK gene and collagen synthesis of the cultured HSFB could be inhibited by FAK ASODN, indicating that FAK played a role in the development of excessive fibrosis of human hypertrophic scar.
