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Presence and function of microRNA-92a in chondrogenic ATDC5 and adipose-derived mesenchymal stem cells.

Hou C, Zhang Z, Zhang Z, Wu P, Zhao X, Fu M, Sheng P, Kang Y, Liao W - Mol Med Rep (2015)

Bottom Line: The expression of miR‑92a was elevated in the chondrogenic ATDC5 cells and hADSCs, and also in the IL‑1β‑induced ATDC5 cells, PMCs and PHCs.Forced expression of miR‑92a enhanced the expression levels of col9a2 and aggrecan.These results demonstrated that miR‑92a was involved in chondrogenesis and the chondrocyte response induced by IL‑1β. miR‑92a positively contributed to the expression of col9a2 and of aggrecan.

View Article: PubMed Central - PubMed

Affiliation: Department of Joint Surgery, The First Affiliated Hospital of Sun Yat‑Sen University, Guangzhou, Guangdong 510080, P.R. China.

ABSTRACT
The aim of the present study was to investigate the presence and biological function of microRNA-92a (miR-92a) in chondrogenesis and cartilage degeneration. Human adipose‑derived mesenchymal stem cells (hADSCs) in micromass and chondrocyte‑like ATDC5 cells were induced to chondrogenesis, and primary human/mouse chondrocytes (PHCs/PMCs) and chondrogenic ATDC5 cells were stimulated with interleukin‑1β (IL‑1β). An miR‑92a mimic/inhibitor was transfected into the ATDC5 cells using lipofectamine 2000. Gene expression was analyzed using reverse transcription‑quantitative polymerase chain reaction. Alcian blue was used to stain the cartilage nodules and chondrogenic micromass. The potential target genes, signaling pathways and functions of miR‑92a were examined using miRanda, miRDB, CLIP‑Seq, TargetScan and Kyoto Encyclopedia of Genes and Genomes. The expression of miR‑92a was elevated in the chondrogenic ATDC5 cells and hADSCs, and also in the IL‑1β‑induced ATDC5 cells, PMCs and PHCs. Forced expression of miR‑92a enhanced the expression levels of col9a2 and aggrecan. A total of 279 genes were predicted as potential target genes of miR‑92a. The phosphoinositide 3‑kinase/PI3K)‑Akt, ErbB and focal adhesion kinase pathways, extracellular matrix (ECM)‑receptor interaction and the mammalian target of rapamycin (mTOR) signaling pathway were suggested to mediate the effects of miR‑92a on chondrogenesis and cartilage degeneration. These results demonstrated that miR‑92a was involved in chondrogenesis and the chondrocyte response induced by IL‑1β. miR‑92a positively contributed to the expression of col9a2 and of aggrecan.

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Experssion of miR-92a in chondrocytes with IL-1β. Error bars indicate the mean ± standard deviation. (A) Expression of miR-92a was elevated in primary mouse chondrocytes treated with 1 ng/ml IL-1β for 4 h. (B) Expression of miR-92a was elevated in primary human chondrocytes treated with 1 ng/ml IL-1β for 4 h. No mmp13 was detected in the control group. (C) Expression of miR-92a was elevated in a time-dependent manner in the chondrogenic ATDC5 cells treated with 1 ng/ml IL-1β. miR-92a, microRNA-92a; IL-1β, interleukin-1β.
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f3-mmr-12-04-4877: Experssion of miR-92a in chondrocytes with IL-1β. Error bars indicate the mean ± standard deviation. (A) Expression of miR-92a was elevated in primary mouse chondrocytes treated with 1 ng/ml IL-1β for 4 h. (B) Expression of miR-92a was elevated in primary human chondrocytes treated with 1 ng/ml IL-1β for 4 h. No mmp13 was detected in the control group. (C) Expression of miR-92a was elevated in a time-dependent manner in the chondrogenic ATDC5 cells treated with 1 ng/ml IL-1β. miR-92a, microRNA-92a; IL-1β, interleukin-1β.

Mentions: Expression levels of miR-92a and mmp13 were upregulated in the PHCs and PMCs treated with 1 ng/ml IL-1β for 4 h, compared with the control (Fig. 3A and B). The expression levels of miR-92a and mmp13 were elevated, and that of col2a1 was suppressed in a time-dependent manner in the chondrogenic ATDC5 cells treated with 1 ng/ml IL-1β (Fig. 3C).


Presence and function of microRNA-92a in chondrogenic ATDC5 and adipose-derived mesenchymal stem cells.

Hou C, Zhang Z, Zhang Z, Wu P, Zhao X, Fu M, Sheng P, Kang Y, Liao W - Mol Med Rep (2015)

Experssion of miR-92a in chondrocytes with IL-1β. Error bars indicate the mean ± standard deviation. (A) Expression of miR-92a was elevated in primary mouse chondrocytes treated with 1 ng/ml IL-1β for 4 h. (B) Expression of miR-92a was elevated in primary human chondrocytes treated with 1 ng/ml IL-1β for 4 h. No mmp13 was detected in the control group. (C) Expression of miR-92a was elevated in a time-dependent manner in the chondrogenic ATDC5 cells treated with 1 ng/ml IL-1β. miR-92a, microRNA-92a; IL-1β, interleukin-1β.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4581768&req=5

f3-mmr-12-04-4877: Experssion of miR-92a in chondrocytes with IL-1β. Error bars indicate the mean ± standard deviation. (A) Expression of miR-92a was elevated in primary mouse chondrocytes treated with 1 ng/ml IL-1β for 4 h. (B) Expression of miR-92a was elevated in primary human chondrocytes treated with 1 ng/ml IL-1β for 4 h. No mmp13 was detected in the control group. (C) Expression of miR-92a was elevated in a time-dependent manner in the chondrogenic ATDC5 cells treated with 1 ng/ml IL-1β. miR-92a, microRNA-92a; IL-1β, interleukin-1β.
Mentions: Expression levels of miR-92a and mmp13 were upregulated in the PHCs and PMCs treated with 1 ng/ml IL-1β for 4 h, compared with the control (Fig. 3A and B). The expression levels of miR-92a and mmp13 were elevated, and that of col2a1 was suppressed in a time-dependent manner in the chondrogenic ATDC5 cells treated with 1 ng/ml IL-1β (Fig. 3C).

Bottom Line: The expression of miR‑92a was elevated in the chondrogenic ATDC5 cells and hADSCs, and also in the IL‑1β‑induced ATDC5 cells, PMCs and PHCs.Forced expression of miR‑92a enhanced the expression levels of col9a2 and aggrecan.These results demonstrated that miR‑92a was involved in chondrogenesis and the chondrocyte response induced by IL‑1β. miR‑92a positively contributed to the expression of col9a2 and of aggrecan.

View Article: PubMed Central - PubMed

Affiliation: Department of Joint Surgery, The First Affiliated Hospital of Sun Yat‑Sen University, Guangzhou, Guangdong 510080, P.R. China.

ABSTRACT
The aim of the present study was to investigate the presence and biological function of microRNA-92a (miR-92a) in chondrogenesis and cartilage degeneration. Human adipose‑derived mesenchymal stem cells (hADSCs) in micromass and chondrocyte‑like ATDC5 cells were induced to chondrogenesis, and primary human/mouse chondrocytes (PHCs/PMCs) and chondrogenic ATDC5 cells were stimulated with interleukin‑1β (IL‑1β). An miR‑92a mimic/inhibitor was transfected into the ATDC5 cells using lipofectamine 2000. Gene expression was analyzed using reverse transcription‑quantitative polymerase chain reaction. Alcian blue was used to stain the cartilage nodules and chondrogenic micromass. The potential target genes, signaling pathways and functions of miR‑92a were examined using miRanda, miRDB, CLIP‑Seq, TargetScan and Kyoto Encyclopedia of Genes and Genomes. The expression of miR‑92a was elevated in the chondrogenic ATDC5 cells and hADSCs, and also in the IL‑1β‑induced ATDC5 cells, PMCs and PHCs. Forced expression of miR‑92a enhanced the expression levels of col9a2 and aggrecan. A total of 279 genes were predicted as potential target genes of miR‑92a. The phosphoinositide 3‑kinase/PI3K)‑Akt, ErbB and focal adhesion kinase pathways, extracellular matrix (ECM)‑receptor interaction and the mammalian target of rapamycin (mTOR) signaling pathway were suggested to mediate the effects of miR‑92a on chondrogenesis and cartilage degeneration. These results demonstrated that miR‑92a was involved in chondrogenesis and the chondrocyte response induced by IL‑1β. miR‑92a positively contributed to the expression of col9a2 and of aggrecan.

Show MeSH
Related in: MedlinePlus