MiR-99b regulates cerebral ischemia neuronal injury through targeting IGF1R

被引:1
作者
Qi, Dengbin [1 ]
Wang, Wei [2 ]
Zhang, Ying [3 ]
Zhang, Tao [4 ]
机构
[1] Jining Med Univ, YanZhou Branch, Affiliated Hosp, Dept Neurol, Jining, Peoples R China
[2] Qingdao Municipal Hosp, Disinfect Supply Ctr, Qingdao, Peoples R China
[3] Binzhou Peoples Hosp, Dept Internal Med, Binzhou, Peoples R China
[4] Shandong First Med Univ, Shandong Prov Hosp, Dept Cardiovasc Surg, Jinan, Shandong, Peoples R China
关键词
Brain ischemia; Receptor; IGF type 1; Apoptosis; INFLAMMATORY RESPONSE; CELL-PROLIFERATION; OXIDATIVE STRESS; BAX/BCL-2; RATIO; CANCER; REPERFUSION; EXPRESSION; MICRORNAS; APOPTOSIS; DEATH;
D O I
10.23736/S0031-0808.20.03920-8
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
BACKGROUND: Recently, microRNA-99b (miR-99b) shows diverse functions in different human disease. However, further studies about the potential effect of miR-99b in cerebral ischemia injury still need to be done. METHODS: The expressions of miR-99b and IGF1R were detected via RT-qPCR assay. Western blot assay was applied to measure the protein expression of Caspase-3, Bax and Bcl-2. MTT assay was used to observe cell viability of SH-SY5Y cells. The association of miR-99b and IGF1R was testified by dual luciferase assay. And human SH-SY5Y cells were treated with the oxygen-glucose deprivation/reperfusion (OGD/R) to mimic CIR injury. RESULTS: The expression of miR-99b was increased in the OGD/R model. And upregulation of miR-99b promoted cell viability and inhibited apoptosis induced by OGD/R. Moreover, IGF1R was confirmed as a direct target gene of miR-99b. The expression of IGF1R was obviously decreased under OGD/R conditions. CONCLUSIONS: MiR-99b promoted the viability and suppressed apoptosis of SH-SY5Y cells under OGD/R conditions through targeting IGF1R.
引用
收藏
页码:30 / 36
页数:7
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