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Effects of miR-30 a on cell cycle and dendritic cell-suppressive function of MSCs / 中国免疫学杂志
Chinese Journal of Immunology ; (12): 462-466,471, 2015.
Article in Chinese | WPRIM (Western Pacific) | ID: wpr-601037
Responsible library: WPRO
ABSTRACT

Objective:

Mesenchymal stem cells( MSCs) have self-renewal capacity and potential to differentiate into the cells.It was reported that the expression of miR-30a changed in some immune diseases.But it remains unclear the effect of miR-30a on the im-munoregulatory functions of MSCs.Here we studied the impact of miR-30a on the phenotype,cell viability,apoptosis,cell cycle and im-munoregulatory functions of MSCs.

Methods:

The mixed enzyme methods were used for the isolation of human umbilical cord MSCs.Flow cytometry(FCM)was used to investigate the effect of overexpressed miR-30a on the phenotype of MSCs.CCK-8 was used to examine the cell viability of miR-30a-overexpressed MSCs.Annexin V/PI was used for the detection of apoptosis of MSCs.Q-PCR and Western blot were used to investigate the effect of miR-30a on the expression of Cyclin E2( CCNE2).CCNE2 was one putative target of miR-30a predicted by Targetscan database.The effects of miR-30a-overexpressed MSCs on the maturation of dendritic cells(DCs)were determined.

Results:

Overexpression of miR-30a blocked the cell cycle of MSCs in the G0/G1 phase by inhibiting the expression of CCNE2,but did not affect the phenotype, cell viability and apoptosis of MSCs.When co-cultured with DCs, although MSCs down-regulated the expression of CD40 and CD86 on DCs,overexpression of miR-30a more significantly enhanced the suppressive impact of MSCs on the maturation of DCs.

Conclusion:

miR-30a affects the cell cycle of MSCs and enhances its immunosuppressive effect on DCs.

Full text: Available Database: WPRIM (Western Pacific) Language: Chinese Journal: Chinese Journal of Immunology Year: 2015 Document type: Article
Full text: Available Database: WPRIM (Western Pacific) Language: Chinese Journal: Chinese Journal of Immunology Year: 2015 Document type: Article
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