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MiR-210 inhibits NF-κB signaling pathway by targeting DR6 in osteoarthritis.

Zhang D, Cao X, Li J, Zhao G - Sci Rep (2015)

Bottom Line: In the in vitro study, miR-210 level in chondrocytes was decreased after treatment with lipopolysaccharide (LPS).MiR-210 expression is reduced in OA rats.The results demonstrated that miR-210 decreased inflammation in articular cavity in OA rats by targeting DR6 and inhibiting NF-κB signaling pathway.

View Article: PubMed Central - PubMed

Affiliation: Department of Orthopedics, Xijing Hospital, Fourth Military Medical University, Xi'an 710032, China.

ABSTRACT
Osteoarthritis (OA) is characterized by degradation of articular cartilage and joint inflammation. MicroRNAs have been proved to play an important role in the regulation of chondrogenesis. Previous study showed that microRNA-210 (miR-210) was probably associated with osteoarthritis, while the function of miR-210 in osteoarthritis still remains unknown. The aim of the present study was to investigate the protective effect of miR-210 on osteoarthritis. In the in vitro study, miR-210 level in chondrocytes was decreased after treatment with lipopolysaccharide (LPS). Transfection with miR-210 mimic inhibited LPS-induced pro-inflammatory cytokines production, cell viability reduction and cell apoptosis. Results of luciferase activity assay showed that miR-210 targeted 3'-UTR of death receptor 6 (DR6) to inhibit its expression. MiR-210 mimic and DR6 siRNA transfection inhibited the activation of NF-κB pathway and cell apoptosis of chondrocytes. For the in vivo study, OA model was established on rats by anterior cruciate ligament transection (ACLT). MiR-210 expression is reduced in OA rats. MiR-210 over-expressing lentivirus was injected into the OA rats. Cytokines production, and NF-κB and DR6 expression in OA rats was inhibited by miR-210 overexpression. The results demonstrated that miR-210 decreased inflammation in articular cavity in OA rats by targeting DR6 and inhibiting NF-κB signaling pathway.

No MeSH data available.


Related in: MedlinePlus

mRNA levels of miR-210 in chondrocytes.(a) MiR-210 mRNA level in chondrocytes with LPS/PBS treatment; (b) MiR-210 mRNA level in chondrocytes transfected with negative mimic or miR-210 mimic. Data are shown as mean ± SD of three experimental replicates. *P < 0.05 vs. control group.
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f1: mRNA levels of miR-210 in chondrocytes.(a) MiR-210 mRNA level in chondrocytes with LPS/PBS treatment; (b) MiR-210 mRNA level in chondrocytes transfected with negative mimic or miR-210 mimic. Data are shown as mean ± SD of three experimental replicates. *P < 0.05 vs. control group.

Mentions: The isolated chondrocytes were treated with LPS to induce inflammation in vitro, the expression level of miR-210 was detected by RT-PCR. As shown in Fig. 1a, the miR-210 level was decreased by 75% in LPS induced cells. To investigate the effect of miR-210 on LPS-induced inflammation in chondrocytes, the isolated chondrocytes were transfected with miR-210 mimic or negative mimic. Expression of miR-210 in chondrocytes was significantly enhanced after transfection with miR-210 mimic (Fig. 1b).


MiR-210 inhibits NF-κB signaling pathway by targeting DR6 in osteoarthritis.

Zhang D, Cao X, Li J, Zhao G - Sci Rep (2015)

mRNA levels of miR-210 in chondrocytes.(a) MiR-210 mRNA level in chondrocytes with LPS/PBS treatment; (b) MiR-210 mRNA level in chondrocytes transfected with negative mimic or miR-210 mimic. Data are shown as mean ± SD of three experimental replicates. *P < 0.05 vs. control group.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4525484&req=5

f1: mRNA levels of miR-210 in chondrocytes.(a) MiR-210 mRNA level in chondrocytes with LPS/PBS treatment; (b) MiR-210 mRNA level in chondrocytes transfected with negative mimic or miR-210 mimic. Data are shown as mean ± SD of three experimental replicates. *P < 0.05 vs. control group.
Mentions: The isolated chondrocytes were treated with LPS to induce inflammation in vitro, the expression level of miR-210 was detected by RT-PCR. As shown in Fig. 1a, the miR-210 level was decreased by 75% in LPS induced cells. To investigate the effect of miR-210 on LPS-induced inflammation in chondrocytes, the isolated chondrocytes were transfected with miR-210 mimic or negative mimic. Expression of miR-210 in chondrocytes was significantly enhanced after transfection with miR-210 mimic (Fig. 1b).

Bottom Line: In the in vitro study, miR-210 level in chondrocytes was decreased after treatment with lipopolysaccharide (LPS).MiR-210 expression is reduced in OA rats.The results demonstrated that miR-210 decreased inflammation in articular cavity in OA rats by targeting DR6 and inhibiting NF-κB signaling pathway.

View Article: PubMed Central - PubMed

Affiliation: Department of Orthopedics, Xijing Hospital, Fourth Military Medical University, Xi'an 710032, China.

ABSTRACT
Osteoarthritis (OA) is characterized by degradation of articular cartilage and joint inflammation. MicroRNAs have been proved to play an important role in the regulation of chondrogenesis. Previous study showed that microRNA-210 (miR-210) was probably associated with osteoarthritis, while the function of miR-210 in osteoarthritis still remains unknown. The aim of the present study was to investigate the protective effect of miR-210 on osteoarthritis. In the in vitro study, miR-210 level in chondrocytes was decreased after treatment with lipopolysaccharide (LPS). Transfection with miR-210 mimic inhibited LPS-induced pro-inflammatory cytokines production, cell viability reduction and cell apoptosis. Results of luciferase activity assay showed that miR-210 targeted 3'-UTR of death receptor 6 (DR6) to inhibit its expression. MiR-210 mimic and DR6 siRNA transfection inhibited the activation of NF-κB pathway and cell apoptosis of chondrocytes. For the in vivo study, OA model was established on rats by anterior cruciate ligament transection (ACLT). MiR-210 expression is reduced in OA rats. MiR-210 over-expressing lentivirus was injected into the OA rats. Cytokines production, and NF-κB and DR6 expression in OA rats was inhibited by miR-210 overexpression. The results demonstrated that miR-210 decreased inflammation in articular cavity in OA rats by targeting DR6 and inhibiting NF-κB signaling pathway.

No MeSH data available.


Related in: MedlinePlus