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Adenovirus-mediated RNA interference against core binding factor alpha 1 inhibits the hypertrophic differentiation of chondrocytes / 中国组织工程研究
Chinese Journal of Tissue Engineering Research ; (53): 187-191, 2015.
Article in Chinese | WPRIM | ID: wpr-462244
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 .

Full text: Available Index: WPRIM (Western Pacific) Language: Chinese Journal: Chinese Journal of Tissue Engineering Research Year: 2015 Type: Article

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Full text: Available Index: WPRIM (Western Pacific) Language: Chinese Journal: Chinese Journal of Tissue Engineering Research Year: 2015 Type: Article