首页> 外文期刊>Journal of biomaterials and tissue engineering >LncRNA Urothelial Carcinoma-Associated 1 (UCA1) Regulates Rat Bone Marrow Mesenchymal Stem Cell Differentiation and Promotes Repair of Bone Defects
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LncRNA Urothelial Carcinoma-Associated 1 (UCA1) Regulates Rat Bone Marrow Mesenchymal Stem Cell Differentiation and Promotes Repair of Bone Defects

机译:LNCRNA尿路上皮癌相关1(UCA1)调节大鼠骨髓间充质干细胞分化并促进骨缺损的修复

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Bone marrow mesenchymal stem cells (BMSCs) have characteristics of self-renewal and multidirectional differentiation. LncRNA UCA1 regulates BMSCs differentiation. Whether LncRNA UCA1 plays a role in bone defects remains unclear. BMSCs were randomly divided into control group, radiation group (6Gy), radiation + UCA1 group followed by analysis of the expression of LncRNA UCA1, RUNX2 and OPN by real time PCR, BMSCs proliferation by MTT assay as well as ALP activity. Healthy Sprague-Dawley rats were randomly divided into control group; bone defect group; UCA1 group, in which UCA1-transfected BMSCs were infused into bone defect rats followed by analysis of bone mineral density, ALP activity as well as the formation of type II collagen by ELISA. LncRNA UCA1 expression was significantly decreased in BMSCs of irradiated group, with decreased BMSCs proliferation, reduced expression of RUNX2 and OPN as well as decreased ALP activity (P < 0.05). Transfection of UCA1 significantly up-regulated LncRNA UCA1 expression in BMSCs, promoted BMSCs proliferation, increased the expression of RUNX2 and OPN, and the activity of ALP (P < 0.05). In addition, UCA1 promoted bone mineral density, increased ALP activity and type II collagen formation in rats with bone defect. LncRNA UCA1 promotes osteogenic differentiation of BMSCs, and targeting it might be a novel approach to promote bone remodeling at the bone defect site.
机译:骨髓间充质干细胞(BMSC)具有自我更新和多向分化的特征。 LNCRNA UCA1调节BMSCs差异化。 LNCRNA UCA1在骨缺损中发挥作用尚不清楚。将BMSCs随机分为对照组,辐射组(6Gy),辐射+ UCA1组,然后通过实时PCR分析LNCRNA UCA1,Runx2和OPN的表达,通过MTT测定和ALP活性进行BMSCs增殖。健康的Sprague-Dawley大鼠随机分为对照组;骨缺陷组; UCA1组,其中UCA1转染的BMSCs注入骨缺损大鼠,然后分析骨矿物密度,ALP活性以及ELISA的II型胶原蛋白的形成。辐照基团的BMSCs中,LNCRNA UCA1表达显着降低,具有降低的BMSC增殖,降低RUNX2和OPN的表达以及降低的ALP活性(P <0.05)。在BMSCs中转染UCA1显着上调的LNCRNA UCA1表达,促进了BMSC的增殖,增加了Runx2和OPN的表达,以及ALP的活性(P <0.05)。此外,UCA1促进了骨缺损大鼠的骨矿物密度,增加的ALP活性和II型胶原蛋白的形成。 LNCRNA UCA1促进BMSCs的成骨分化,并靶向它可能是促进骨缺损部位骨质重塑的新方法。

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