Adenovirus-mediated RNA interference against core binding factor alpha 1 inhibits the hypertrophic differentiation of chondrocytes
10.3969/j.issn.2095-4344.2015.02.005
- VernacularTitle:腺病毒介导RNA干扰抑制核心结合因子α1表达阻断软骨细胞的肥大分化
- Author:
Bo GAO
;
Rong XING
;
Qingquan KONG
;
Zhou XIANG
;
Jing YANG
;
Jiaqin CAI
;
Yizhou HUANG
;
Xiuqun LI
;
Xiaohe CHEN
- Publication Type:Journal Article
- Keywords:
Chondrocytes;
Core Binding Factors;
RNA Interference;
Adenoviridae
- From:
Chinese Journal of Tissue Engineering Research
2015;(2):187-191
- CountryChina
- Language:Chinese
-
Abstract:
BACKGROUND:Hypertrophic differentiation of chondrocytes is the sign of starting endochondral ossification, and it is also an essential step in endochondral ossification, which is a cascade reaction and difficult to be blocked once started. The end result is the formation of bone structure. RNA interference is a post-transcriptional gene silencing. Relevant studies have shown that the use of RNA interference to block the expression of core binding factorα1 (Cbfα1) can effectively inhibit the formation of heterotopic ossification. OBJECTIVE:To use RNA intereference technology to suppress Cbfα1 expression so as to achieve the purpose of blocking the hypertrophic diferentiation of chondrocytes. METHODs: We constructed an adenovirus containing siRNA against Cbfα1 (Ad-Cbfα1-siRNA). Retinoic acid and interleukin-1α were used to induce hypertrophic differetiation of chondrocytes, and then Ad-Cbfα1-siRNA was utilized to inhibit the hypertrophic differentiation of chondrocytes. Immunohistochemistry method was used to analyze the expression of Cbfα1. RESULTS AND CONCLUSION:After induction with retinoic acid and interleukin-1α, the chondrocytes in the negative control virus group appeared to have hypertrophy and the expression of Cbfα1 was positive. In the Ad-Cbα1-siRNA group, the expression of Cbfα1 was negative. These findings suggest that the inhibition of Cbfα1 by RNA interference can be a powerful way to prevent the hypertrophic differentiation of chondrocytes .
