LncRNA Small Nucleolar RNA Host Gene 11 (SNHG11) Participates in Hypoxia/Reoxygenation-Induced Adrenal Phaeochromocytoma (PC12) Cell Damage in a ceRNA-Dependent Manner

Author:

Du Jinlong1,Gu Huiqin1,Cai Shan1

Affiliation:

1. Department of Critical Care Medicine, Xianning Central Hospital, The First Affiliated Hospital of Hubei University of Science and Technology, Xianning, Hubei, 437000, China

Abstract

How to prevent cerebral ischemia-reperfusion injury (CI/R) is critical for treating ischemic stroke. LncRNA SNHG11 can participate in several diseases by competing endogenous RNA (ceRNA), but its’ role in CI/R is unclear. Hypoxia/reoxygenation model (H/R group) cells were set and separated into control team; H/R team; H/R+SNHG11 team and H/R+si-SNHG11 team followed by analysis of LncRNA SNHG11 by real-time PCR, LncRNA SNHG11 subcellular distribution by FISH assay, MTT assay for cell proliferation, flow cytometry for apoptosis, ROS and LDH content and PTEN expression by Western blot. In H/R group, SNHG11 level significantly increased and cell proliferation significantly decreased, along with increased cell apoptosis, ROS activity, LDH content and PTEN expression in comparison of control group (P-value less than 0.05); The foregoing variation was promoted further by the H/R group after overexpression of SNHG11 (P-value below 0.05) and reversed after transfection of SNHG1 siRNA (P <0.05). LncRNA SNHG11 is mainly localized on the cell membrane. miR-16 is a SNHG11 targeted miRNA. Transfection of miR-16 mimics into PC12 cells in H/R group can significantly promote cell proliferation, inhibit apoptosis, reduce ROS activity, LDH content and PTEN expression versus the H/R group (P-value less than 0.05). SNHG11 level in H/R condition is increased and might target miR-16 to regulate PTEN expression and oxidative stress, leading to apoptosis and damage.

Publisher

American Scientific Publishers

Subject

Biomedical Engineering,Medicine (miscellaneous),Bioengineering,Biotechnology

同舟云学术

1.学者识别学者识别

2.学术分析学术分析

3.人才评估人才评估

"同舟云学术"是以全球学者为主线,采集、加工和组织学术论文而形成的新型学术文献查询和分析系统,可以对全球学者进行文献检索和人才价值评估。用户可以通过关注某些学科领域的顶尖人物而持续追踪该领域的学科进展和研究前沿。经过近期的数据扩容,当前同舟云学术共收录了国内外主流学术期刊6万余种,收集的期刊论文及会议论文总量共计约1.5亿篇,并以每天添加12000余篇中外论文的速度递增。我们也可以为用户提供个性化、定制化的学者数据。欢迎来电咨询!咨询电话:010-8811{复制后删除}0370

www.globalauthorid.com

TOP

Copyright © 2019-2024 北京同舟云网络信息技术有限公司
京公网安备11010802033243号  京ICP备18003416号-3