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Long non?coding RNA SNHG16 inhibits the oxygen?glucose deprivation and reoxygenation?induced apoptosis in human brain microvascular endothelial cells by regulating miR?15a?5p/bcl?2.

ABSTRACT: MicroRNA (miR) 15a?5p can promote ischemia/reperfusion (I/R)?induced apoptosis of cerebral vascular endothelial cells, which is inhibited by long non?coding RNAs (lncRNAs). The present study investigated the potential of lncRNAs targeting miR?15a?5p to regulate oxygen?glucose deprivation and reoxygenation (OGD?R)?induced apoptosis of human brain microvascular endothelial cells (hBMECs). hBMECs were transfected with or without miR?15a?5p or its mutant, together with p?small nucleolar RNA host gene 16 (SNHG16) or its mutant. Following OGD?R, proliferation, apoptosis and miR?15a?5p, SNHG16 and Bcl?2 expression levels were determined using MTT, flow cytometry, reverse transcription?quantitative PCR or western blotting. The potential interaction of SNHG16 with miR?15a?5p was analyzed by pull?down, luciferase and immunoprecipitation assays. OGD?R induced apoptosis of hBMECs and increased miR?15a?5p expression levels in a time?dependent manner. miR?15a?5p overexpression decreased the proliferation of hBMECs and promoted apoptosis by decreasing Bcl?2 expression levels. SNHG16 was pulled?down by miR?15a?5p and anti?Ago2. miR?15a?5p overexpression significantly decreased SNHG16?regulated luciferase activity and hBMEC survival by increasing apoptosis. SNHG16 overexpression decreased miR?15a?5p expression levels in hBMECs. SNHG16 gradually decreased following OGD?R and its overexpression decreased miR?15a?5p expression levels and promoted the proliferation of hBMECs by decreasing apoptosis. SNHG16 enhanced Bcl?2 expression levels in hBMECs, which was abrogated by miR?15a?5p. Bioinformatics suggest that SNHG16 may antagonize the binding of miR?15a?5p to the 3'UTR of Bcl?2 mRNA. These findings suggest that SNHG16 may protect hBMECs from OGD?R?induced apoptosis by antagonizing the miR?15a?5p/bcl?2 axis. Thus, targeting SNHG16?based mechanisms may provide novel therapeutic strategies for treatment of ischemic stroke.

SUBMITTER: Teng H

PROVIDER: S-EPMC7453539 | biostudies-literature | 2020 Jul

REPOSITORIES: biostudies-literature

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Long non‑coding RNA SNHG16 inhibits the oxygen‑glucose deprivation and reoxygenation‑induced apoptosis in human brain microvascular endothelial cells by regulating miR‑15a‑5p/bcl‑2.

Teng Hongwei H Li Ming M Qian Lei L Yang Hua H Pang Mingzhi M

Molecular medicine reports 20200729 4

MicroRNA (miR) 15a‑5p can promote ischemia/reperfusion (I/R)‑induced apoptosis of cerebral vascular endothelial cells, which is inhibited by long non‑coding RNAs (lncRNAs). The present study investigated the potential of lncRNAs targeting miR‑15a‑5p to regulate oxygen‑glucose deprivation and reoxygenation (OGD‑R)‑induced apoptosis of human brain microvascular endothelial cells (hBMECs). hBMECs were transfected with or without miR‑15a‑5p or its mutant, together with p‑small nucleolar RNA host gen ...[more]

PMID: 32945414

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Project description:BackgroundDeep hypothermic circulatory arrest (DHCA) is a technique used during the surgical treatment of aneurysms of the thoracic aorta in adult patients, and complex congenital heart disease in neonates. And brain microvascular endothelial cells (BMECs) are essential components of the cerebrovascular network and participate in maintaining the blood-brain barrier (BBB) and brain function. In our previous study, we found that oxygen-glucose deprivation and reoxygenation (OGD/R) activated Toll-like receptor 4 (TLR4) signaling in BMECs, and induced pyroptosis and inflammation. In this study, we further investigated the potential mechanism of ethyl(6R)-6-[N-(2-Chloro-4-fluorophenyl) sulfamoyl] cyclohex-1-ene-1-carboxylate (TAK-242) on BMECs under OGD/R, as in patients with sepsis, the TAK-242 was tested in clinical trials.MethodsTo confirm the function of TAK-242 on BMECs under OGD/R, cell viability, inflammatory factors, inflammation-associated pyroptosis, and nuclear factor-κB (NF-κB) signaling were determined using Cell Counting Kit-8 (CCK-8) assay, enzyme-linked immunosorbent assay (ELISA), and western blotting, respectively. To investigate the lncRNAs associated with TLR4 during OGD/R, long non-coding RNAs (lncRNAs) and messenger RNAs (mRNAs) expression patterns were profiled with RNA deep sequencing. Moreover, to confirm whether lncRNA-encoded short peptides, liquid chromatography-tandem mass spectrometry (LC-MS/MS) was used.ResultsRelative control group, OGD/R inhibited the cell viability, increased the section of inflammatory factors secretion, including IL-1β, IL-6, and TNF-α, and promoted the pathways of TLR4/NLRP3/Caspase-1 and TLR4/NF-κB. However, TAK-242 + OGD/R group promoted OGD/R cell viability, decreased OGD/R-induced inflammatory factors secretion, and inhibited the pathways of TLR4/NLRP3/Caspase-1 and TLR4/NF-κB. In addition, AABR07000411.1, AABR070006957.1, and AABR070008256.1 were decreased in OGD/R cells compared with controls, but TAK-242 restored their expression under OGD/R condition. AABR07000473.1, AC130862.4, and LOC10254972.6 were induced by OGD/R, but were suppressed in TAK-242 + OGD/R cells compared with OGD/R. Moreover, AABR07049961.1, AC127076.2, AABR07066020.1, and AABR07025303.1-encoded short peptides were dysregulated in OGD/R cells, and TAK-242 attenuated the dysregulation of AABR07049961.1, AC127076.2, and AABR07066020.1-encoded short peptides.ConclusionsTAK-242 alters the expression pattern of lncRNAs in OGD/R cells, and differently expressed lncRNAs may exert a protective effect against OGD/R injury through a mechanism of competing endogenous RNA (ceRNA) and encoding short peptides. These findings maybe provide a new theory basis for the treatment of DHCA.

Project description:The aim of the present study was to explore the effects of LINC00649 on the proliferation, migration and invasion of bladder cancer (BC) and identify possible mechanisms. Through TCGA database analysis of LINC00649 expression in bladder cancer and the association of LINC00649 with the BC patient prognosis, RT‑qPCR was employed for detecting LINC00649 expression in 60 clinical tissue specimens and cell lines of bladder cancer. The lentivirus stable transfection or small interfering RNA was used to increase or decrease the LINC00649 expression level in T24 and UM‑UC‑3 cells. CCK8 and clone formation assay were utilized to observe the effects of LINC00649 on the proliferation and colony formation of BC cells. Transwell experiment was performed to detect the effects of LINC00649 on the migration and invasion of bladder cancer. Bioinformatics database was used to identify the possible downstream targets of LINC00649 while RT‑qPCR, western blot analysis and dual luciferase reporter gene experiments were carried out to verify the possible molecular mechanism. The TCGA database analysis revealed a significantly high expression of LINC00649 in bladder cancer and an association of LINC00649 expression with overall survival rate of BC patients. As shown by RT‑qPCR detection, LINC00649 expression was notably upregulated in BC tissues and BC cell lines. In addition, statistical analyses unveiled that highly expressed LINC00649 was clearly associated with poor overall survival of bladder cancer. Based on the in vitro cell experiment, upregulated LINC00649 considerately enhanced the proliferation, migration and invasion of BC cells, as opposed to those in T24 and UM‑UC‑3 cells by suppressing LINC00649. Mechanically, LINC00649 may promote the malignant progression of bladder cancer by regulating miR‑15a‑5p to promote the HMGA1 expression axis. Overall, LINC00649 upregulates HMGA1 expression by binding to miR‑15a‑5p to enhance the proliferation, migration and invasion of BC cells. Thus, LINC00649 is a potential biomarker and therapeutic target for bladder cancer.

Dataset Information

Long non?coding RNA SNHG16 inhibits the oxygen?glucose deprivation and reoxygenation?induced apoptosis in human brain microvascular endothelial cells by regulating miR?15a?5p/bcl?2.

Publications

Long non‑coding RNA SNHG16 inhibits the oxygen‑glucose deprivation and reoxygenation‑induced apoptosis in human brain microvascular endothelial cells by regulating miR‑15a‑5p/bcl‑2.

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