Silencing microRNA-34a inhibits chondrocyte apoptosis in a rat osteoarthritis model in vitro

被引：136

作者：

Abouheif, Mohamed M. ^{[1
,2
]}

Nakasa, Tomoyuki ^{[1
]}

Shibuya, Hayatoshi ^{[1
]}

Niimoto, Takuya ^{[1
]}

Kongcharoensombat, Wirat ^{[1
]}

Ochi, Mitsuo ^{[1
]}

机构：

[1] Hiroshima Univ, Dept Orthopaed Surg, Grad Sch Biomed Sci, Minami Ku, Hiroshima 7348551, Japan

[2] Univ Alexandria, Dept Orthoped Surg & Traumatol, Fac Med, El Hadra Univ Hosp, Alexandria, Egypt

来源：

RHEUMATOLOGY | 2010年 / 49卷 / 11期

关键词：

miRNA-34a; Chondrocyte apoptosis; miRNA-34a-specific locked nucleotide analogue; Osteoarthritis; HUMAN ARTICULAR CHONDROCYTES; CHRONIC LYMPHOCYTIC-LEUKEMIA; NITRIC-OXIDE; EXPRESSION PROFILES; CARTILAGE; MIR-34A; IDENTIFICATION; BIOGENESIS; PATHWAY; GENES;

D O I：

10.1093/rheumatology/keq247

中图分类号：

R5 [内科学];

学科分类号：

1002 ; 100201 ;

摘要：

Methods. Locked nucleotide analogue (LNA)-modified miR-34a-specific anti-sense was transfected into rat chondrocyte monolayer culture. After that, IL-1 beta was added to the chondrocytes to create an OA model in vitro. The effect of silencing miR-34a on the prevention of chondrocyte apoptosis was analysed by assessment of the expression levels of Col2a1 and iNOS, also through assessment of cell viability and TUNEL staining. Results. The expression of miR-34a was significantly up-regulated by IL-1 beta. Silencing of miR-34a significantly prevented IL-1 beta-induced down-regulation of Col2a1, as well as IL-1 beta-induced up-regulation of iNOS. Finally, MiR-34a inhibitor could also reduce TUNEL-positive cells. Conclusion. Silencing of miR-34a by LNA-modified anti-sense could effectively reduce rat chondrocyte apoptosis induced by IL-1 beta. This present study revealed that silencing of miR-34a might develop a novel intervention for OA treatment through the prevention of cartilage degradation.

引用

页码：2054 / 2060

页数：7

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