Exogenous micro-RNA and antagomir modulate osteogenic gene expression in tenocytes

被引:6
|
作者
Xiao, Michelle [1 ]
Iglinski-Benjamin, Kag C. [1 ]
Sharpe, Orr [1 ,2 ]
Robinson, William H. [1 ,2 ]
Abrams, Geoffrey D. [1 ,2 ]
机构
[1] Stanford Univ, Sch Med, Dept Orthoped Swgery, Stanford, CA 94305 USA
[2] Vet Affairs Palo Alto Hlth Care Syst, Palo Alto, CA USA
关键词
Micro-RNA; Tenocyte; Tendinopathy; Inflammation; Collagen; EXTRACELLULAR-MATRIX; FAMILY-MEMBERS; TENDON; DIFFERENTIATION; IDENTIFICATION; TENDINOPATHY; MECHANISMS; CELLS;
D O I
10.1016/j.yexcr.2019.03.008
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Tendinopathy is a common and disabling condition that is difficult to treat. The pathomolecular events behind tendinopathy remain uncertain. Micro-RNAs (miRNAs, miRs) are short non-coding RNAs that regulate gene expression and may play a role in tendinopathy development. Tenocytes were obtained from human patellar tendons in patients undergoing anterior cruciate ligament (ACL) reconstruction. Micro-RNA mimics and antagomirs for miR-30d, 26a, and 29a were separately transfected into tenocyte culture. Gene expression for scleraxis, collagen 1 alpha 1 (COL1A1), collagen 3 alpha 1 (COL3A1), interleukin-1-beta (IL-1 beta), interleukin-6 (IL-6), bone morphogenic protein 2 (BMP2), bone morphogenic protein 12 (BMP12), and osteocalcin was determined for each miRNA mimic and antagomir transfection using real-time quantitative PCR (qPCR). The results showed that exogenous miR-29a downregulated BMP2 and BMP12, while miR-26a and miR-30d did not have a significant effect on tenocyte gene expression. These findings suggest miR-29a contributes to tendon homeostasis and can serve as a potential therapeutic target in treating tendinopathy.
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页码:119 / 123
页数:5
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