Home > Journals > Panminerva Medica > Past Issues > Articles online first > Panminerva Medica 2020 Apr 28

CURRENT ISSUE
 

JOURNAL TOOLS

eTOC
To subscribe
Submit an article
Recommend to your librarian
 

ARTICLE TOOLS

Publication history
Reprints
Permissions
Cite this article as

 

 

Panminerva Medica 2020 Apr 28

DOI: 10.23736/S0031-0808.20.03920-8

Copyright © 2020 EDIZIONI MINERVA MEDICA

language: English

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

QI DENGBIN 1, Wang WEI 2, Zhang YING 3, Zhang TAO 4

1 Department of Neurology, Affiliated Hospital of Jining Medical University, YanZhou Branch, Jining, P.R. China; 2 Disinfection Supply Center, Qingdao Municipal Hospital, Qingdao, P.R. China; 3 Department of Internal Medicine, Binzhou People's Hospital, Binzhou, P.R. China; 4 Department of Cardiovascular Surgery, Provincial Hospital Affiliated to Shandong University, Jinan, P.R. China


PDF


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.


KEY WORDS: miR-99; Cerebral ischemia injury; IGF1R; Apoptosis

top of page