机构地区:[1]Repair Department of Stomatology,School of Stomatology,Lanzhou University [2]Department of Stomatology,Gansu Provincial Maternity and Child-care Hospital [3]Polymeric Chemistry and Physics,College of Chemistry and Chemical Engineering,Lanzhou University
出 处:《Asian Pacific Journal of Tropical Medicine》2015年第6期501-504,共4页亚太热带医药杂志(英文版)
基 金:supported by the Fundamental Research Funds for the Central Universities(Izujbky-2014-161)
摘 要:Objective:To explore the effect of microRNA-101 on apoptosis of condylar cartilage cells and the specific mechanism of molecular biology.Methods:IL-1 was used to stimulate and establish the model of apoptosis of condylar cartilage cells.The expression change of miR-101 in control group was compared with that in IL-1 stimulation group by qRT-PCR.Overexpression and down-regulation models of miR-101 were established by transfecting Mimics and Inhibitor and verified by qRT-PCR.Flow cytometry was used to detect the effect of miR-101 overexpression and down-regulation on apoptosis.Target gene of miR-101 was analyzed and calculated through bioinformatics.Western blot and Luciferase report assay were used to detect whether.Sox9 could become the target gene of miR-101.Results:qRTPCR results showed that IL-1 stimulation could cause the increase of miR-101 expression.After the transfection of rabbit condylar cartilage cells by Mimics and Inhibitor,qRT-PCR results confirmed the significant effect of miR-101 overexpression and down-regulation.It was confirmed by flow cytometry that overexpression of miR-101 could promote the apoptosis of condylar cartilage cells,and down-regulation of miR-101 could reduce the apoptosis.It was confirmed by Western blot and Luciferase report assay that Sox9 was the target gene of miR-101.and miR-101 inhibited SOX9 expression through complementary pairing with 3'UTR of Sox9 mRNA.Conclusions:miR-101 can promote the apoptosis of condylar cartilage cells through inhibiting the protein level of target gene S0X9.Objective:To explore the effect of microRNA-101 on apoptosis of condylar cartilage cells and the specific mechanism of molecular biology.Methods:IL-1 was used to stimulate and establish the model of apoptosis of condylar cartilage cells.The expression change of miR-101 in control group was compared with that in IL-1 stimulation group by qRT-PCR.Overexpression and down-regulation models of miR-101 were established by transfecting Mimics and Inhibitor and verified by qRT-PCR.Flow cytometry was used to detect the effect of miR-101 overexpression and down-regulation on apoptosis.Target gene of miR-101 was analyzed and calculated through bioinformatics.Western blot and Luciferase report assay were used to detect whether.Sox9 could become the target gene of miR-101.Results:qRTPCR results showed that IL-1 stimulation could cause the increase of miR-101 expression.After the transfection of rabbit condylar cartilage cells by Mimics and Inhibitor,qRT-PCR results confirmed the significant effect of miR-101 overexpression and down-regulation.It was confirmed by flow cytometry that overexpression of miR-101 could promote the apoptosis of condylar cartilage cells,and down-regulation of miR-101 could reduce the apoptosis.It was confirmed by Western blot and Luciferase report assay that Sox9 was the target gene of miR-101.and miR-101 inhibited SOX9 expression through complementary pairing with 3’UTR of Sox9 mRNA.Conclusions:miR-101 can promote the apoptosis of condylar cartilage cells through inhibiting the protein level of target gene S0X9.
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