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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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Predicted signaling pathways mediating the effects of miR-92a on chondrogenesis and cartilage degeneration. Predicted potential target genes of miR-92a are indicated by the red boxes. (A) PI3K-Akt, (B) ErbB and (C) focal adhesion signaling pathways were predicted based on the potential target genes of miR-92a. miR-92a, microRNA-92a; PI3K, phosphoinositide-3 kinase; mTOR, mammalian target of rapamycin. Predicted signaling pathways mediating the effects of miR-92a on chondrogenesis and cartilage degeneration. Predicted potential target genes of miR-92a are indicated by the red boxes. (D) ECM-receptor interaction and (E) mTOR signaling pathways were predicted based on the potential target genes of miR-92a. miR-92a, microRNA-92a; PI3K, phosphoinositide-3 kinase; mTOR, mammalian target of rapamycin.
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f5-mmr-12-04-4877: Predicted signaling pathways mediating the effects of miR-92a on chondrogenesis and cartilage degeneration. Predicted potential target genes of miR-92a are indicated by the red boxes. (A) PI3K-Akt, (B) ErbB and (C) focal adhesion signaling pathways were predicted based on the potential target genes of miR-92a. miR-92a, microRNA-92a; PI3K, phosphoinositide-3 kinase; mTOR, mammalian target of rapamycin. Predicted signaling pathways mediating the effects of miR-92a on chondrogenesis and cartilage degeneration. Predicted potential target genes of miR-92a are indicated by the red boxes. (D) ECM-receptor interaction and (E) mTOR signaling pathways were predicted based on the potential target genes of miR-92a. miR-92a, microRNA-92a; PI3K, phosphoinositide-3 kinase; mTOR, mammalian target of rapamycin.

Mentions: In addition to RT-qPCR, KEGG analysis was used to investigate the signaling pathways by which miR-92a may regulate chondrogenesis, based on the predicted potential target genes. The potential target genes were clustered based on their involvement in signaling pathways, and signaling pathways, which have been previously identified to be involved in chondrogenesis or cartilage degeneration were selected (5,22–25). The P-value was determined based on the number of potential target genes and the number of total genes in each signaling pathway. Of all of the predicted signaling pathways, the PI3K-Akt (P=0.064), ErbB (P=0.076) and focal adhesion kinase pathways (P=0.014), ECM-receptor interaction (P=0.024) and the mTOR signaling pathway (P=0.007) were identified as significant (Table III, Fig. 5).


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)

Predicted signaling pathways mediating the effects of miR-92a on chondrogenesis and cartilage degeneration. Predicted potential target genes of miR-92a are indicated by the red boxes. (A) PI3K-Akt, (B) ErbB and (C) focal adhesion signaling pathways were predicted based on the potential target genes of miR-92a. miR-92a, microRNA-92a; PI3K, phosphoinositide-3 kinase; mTOR, mammalian target of rapamycin. Predicted signaling pathways mediating the effects of miR-92a on chondrogenesis and cartilage degeneration. Predicted potential target genes of miR-92a are indicated by the red boxes. (D) ECM-receptor interaction and (E) mTOR signaling pathways were predicted based on the potential target genes of miR-92a. miR-92a, microRNA-92a; PI3K, phosphoinositide-3 kinase; mTOR, mammalian target of rapamycin.
© Copyright Policy - open-access
Related In: Results  -  Collection

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

f5-mmr-12-04-4877: Predicted signaling pathways mediating the effects of miR-92a on chondrogenesis and cartilage degeneration. Predicted potential target genes of miR-92a are indicated by the red boxes. (A) PI3K-Akt, (B) ErbB and (C) focal adhesion signaling pathways were predicted based on the potential target genes of miR-92a. miR-92a, microRNA-92a; PI3K, phosphoinositide-3 kinase; mTOR, mammalian target of rapamycin. Predicted signaling pathways mediating the effects of miR-92a on chondrogenesis and cartilage degeneration. Predicted potential target genes of miR-92a are indicated by the red boxes. (D) ECM-receptor interaction and (E) mTOR signaling pathways were predicted based on the potential target genes of miR-92a. miR-92a, microRNA-92a; PI3K, phosphoinositide-3 kinase; mTOR, mammalian target of rapamycin.
Mentions: In addition to RT-qPCR, KEGG analysis was used to investigate the signaling pathways by which miR-92a may regulate chondrogenesis, based on the predicted potential target genes. The potential target genes were clustered based on their involvement in signaling pathways, and signaling pathways, which have been previously identified to be involved in chondrogenesis or cartilage degeneration were selected (5,22–25). The P-value was determined based on the number of potential target genes and the number of total genes in each signaling pathway. Of all of the predicted signaling pathways, the PI3K-Akt (P=0.064), ErbB (P=0.076) and focal adhesion kinase pathways (P=0.014), ECM-receptor interaction (P=0.024) and the mTOR signaling pathway (P=0.007) were identified as significant (Table III, Fig. 5).

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