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Hypoxia-induced shift in the phenotype of proteasome from 26S toward immunoproteasome triggers loss of immunoprivilege of mesenchymal stem cells

机译:缺氧诱导的蛋白酶体表型从26s朝向免疫促粒子触发间充质干细胞的免疫促进

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摘要

Human bone marrow-derived MSCs were incubated in hypoxia chamber for 24 h. a Protein levels of PSMD11, PSMD4 (Rpn10), PSMB6 (β1), PSMB7 (β2), and PSMB5 (β5) as measured by Western blot showed a significant decrease in hypoxic MSCs compared to normoxic cells; n = 3. b, c Immunofluorescence images exhibited a significant decrease in the expression of PSMD4 (Rpn10), PSMD11, PSMB6 (β1), PSMB7 (β2) and PSMB5 (β5) in hypoxic MSCs compared to normoxic cells; n = 4. *p < 0.05 compared to normoxic MSCs. Each experiment was repeated 3–4 times.
机译:将人骨髓衍生的MSCs在缺氧室中孵育24小时。通过Western印迹测量的PSMD11,PSMD4(RPN10),PSMB6(β1),PSMB7(β2)和PSMB5(β5)的蛋白质水平显示出与常氧细胞相比的缺氧MSC的显着降低; N = 3.b,与常氧别细胞相比,C免疫荧光图像表现出PSMD4(RPN10),PSMD11,PSMB6(β1),PSMB7(β2),PSMB7(β2)和PSMB5(β5)的表达显着降低; n = 4. * p <0.05与常氧mscs相比。每次实验重复3-4次。

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