Abstract | OBJECTIVE: METHODS: AIS cell model was constructed by oxygen glucose deprivation and reoxygenation (OGD/R). The quantitative real-time PCR was used to detect the expression of lnc ITSN1-2 in HT22 cells. The effects of lnc ITSN1-2 overexpression or knockdown on viability, LDH release, apoptosis, inflammatory and apoptotic factor expressions in OGD/R-induced HT22 cells were measured by cell counting kit-8 assay, LDH release kit, flow cytometry, ELISA and western blot, respectively. Starbase was used to screen the target genes of lnc ITSN1-2. The targeting relationship between lnc ITSN1-2 and miR-195-5p was predicted by starbase and verified by dual- luciferase report assay. The above assays were conducted again to study the function of miR-195-5p. Lastly, the levels of activated mitogen-activated protein kinases (MAPK) pathway-related proteins were determined by western blot. RESULTS: OGD/R treatment reduced the HT22 cell viability and enhanced LDH release rate and lnc ITSN1-2 expression. Lnc ITSN1-2 overexpression promoted the cell injury, apoptosis and inflammation in OGD/R-induced HT22 cells, while lnc ITSN1-2 knockdown generated the opposite effect and deactivated the MAPK pathways. However, the effect of lnc ITSN1-2 knockdown in OGD/R-induced HT22 cells was reversed by miR-195-5p inhibitor. CONCLUSION: Lnc ITSN1-2 knockdown suppressed the inflammation and apoptosis in OGD/R-induced HT22 cells by regulating the miR-195-5p-mediated MAPK pathways.
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Authors | Fei Zhu, Ermin Luo, Fei Yi, Jianzhong Xiong, Chun Huang, Runying Li |
Journal | Neuroreport
(Neuroreport)
Vol. 32
Issue 16
Pg. 1325-1334
(11 02 2021)
ISSN: 1473-558X [Electronic] England |
PMID | 34554938
(Publication Type: Journal Article)
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Copyright | Copyright © 2021 Wolters Kluwer Health, Inc. All rights reserved. |
Chemical References |
- Adaptor Proteins, Vesicular Transport
- MicroRNAs
- RNA, Long Noncoding
- intersectin 1
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Topics |
- Adaptor Proteins, Vesicular Transport
(genetics, metabolism)
- Animals
- Apoptosis
(physiology)
- Brain Ischemia
(genetics, metabolism)
- Cell Survival
(physiology)
- Gene Knockdown Techniques
- Hippocampus
(metabolism)
- Inflammation
(genetics, metabolism)
- Mice
- MicroRNAs
(genetics, metabolism)
- Neurons
(metabolism)
- RNA, Long Noncoding
(genetics)
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