凋亡目的 分析miR-221-3p靶向基质金属蛋白酶抑制因子-2(TIMP-2)对腹主动脉瘤(AAA)血管平滑肌细胞(VSMC)增殖和凋亡的影响.方法 对人VSMC细胞进行培养,10 μmol/L血管紧张素(AngII)对VSMC进行处理,将VSMC细胞分为miR-221-3p inhibitor组(转染miR-221-3p inhibitor),阴性对照组(转染miR-221-3p inhibitor NC)...
转移的关系,瞬时转染miR-221-3p inhibitor观察其对PTC细胞BCPAP的增殖和凋亡的影响,生物信息学方法分析miR-221-3p可能作用的靶基因、参与的通路及功能.方法:(1)原位杂交法(ISH)检测PTC、滤泡状甲状腺癌(FTC)与正常甲状腺组织中miR-221-...
The qRT-PCR experiment revealed the highest miR-221-3p expression in the miR-221-3p mimics group and the lowest miR-221-3p expression in the miR-221-3p inhibitor group, confirming that the transfection was successful (Figure 8(b)). Moreover, in the HUVEC oxidative stress injury model (...
参与脂肪细胞的分化是miRNA最早被发现的功能之一,为了探讨miR-221-3p对家兔脂肪细胞的分化是否有调控作用,试验以家兔前体脂肪细胞为试验材料,利用人工合成的miR-221-3p mimic,inhibitor及siRNA转染进细胞,检测诱导分化过程中细胞内脂滴的含量及成脂标志基因的m RNA表达水平的变化,预测miR-221-3p与靶基因之间潜在的关系...
增殖凋亡迁移侵袭目的:探讨miR-221-3p是否通过靶向FGF14调节肺腺癌细胞增殖,凋亡,迁移及侵袭的生物学行为.方法:采用qRT-PCR法与Western blot法分别检测人支气管上皮细胞(BEAS-2B),人肺腺癌细胞(A549,A-427,PC-9)中miR-221-3p,FGF14的表达水平;分别将miR-inhibitor-NC,miR-221-3p inhibitor,si-NC,si-FGF14...
In addition, we further confirmed that Ang-2 played a dominant role in miR-221-3p inhibitors promoting the transformation of HCMECs to tip cells by using Ang-2 shRNA to interfere with miR-221-3p inhibitor-treated HCMECs under hypoxic conditions. Finally, we found that miR-221-3p expression...
Using Stattic, a small-molecule inhibitor of STAT3, we observed a significant enhancement in the inhibitory effect of Gefitinib on the growth, migration, and invasion of MDA-MB-231 cells. Additionally, Stattic treatment upregulated miR-221-3p expression and downregulated FSCN1 mRNA and protein ...
BMSCs and CC cells were co-cultured, and transfected with miR-221-3pinhibitor followed by analysis of miR-221-3p level by real time PCR, cell proliferation, apoptosis activity, E-cadherin and Vimentin level, TGF-β1 secretion by ELISA as well as Smad1 and Smad2 expression. BMSCs up...
miR-221-3p or its inhibitor were transfected into differentiating or mature human adipocytes. Triglyceride (TG) content and adipogenic gene expression were monitored, global lipidome analysis was carried out, and mechanisms underlying the effects of miR-221-3p were investigated. Finally, cross-talk ...
The 16HBECs were, additionally, transfected by miR-221-3p mimic, miR-92a-3p mimic, miR-221-3p inhibitor or miR-92a-3p inhibitor, and cytokines released by them, including TNF-α, IL-8, IL-1β, and TGF-β1, were monitored using enzyme linked immunosorbent assay (ELISA) kits. Results...