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LncRNA SNHG15 regulates hypoxic-ischemic brain injury via miR-153-3p/SETD7 axis

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Date
2022
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Authors
Fu, Jiding ; Huang, Yunbo ; Xian, Lewu
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Publisher
Universidad de Murcia, Departamento de Biologia Celular e Histiologia
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DOI
https://doi.org/10.14670/HH-18-489
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info:eu-repo/semantics/article
Description
CORRIGENDUM TO: "LncRNA SNHG15 regulates hypoxic-ischemic brain injury via miR-153-3p/SETD7 axis" Histol Histopathol. 2022 Nov;37(11):1113-1125. doi: 10.14670/HH-18-489
Abstract
Hypoxic-ischemic encephalopathy (HIE) is a leading cause of fatality and morbidity in newborns. Long non-coding RNAs (lncRNAs) Small Nucleolar RNA Host Gene 15 (SNHG15) was elevated in the peripheral blood of patients with acute cerebral ischemia, but its role in HI brain injury remained elusive. Hence, this study aimed to investigate the effect of SNHG15 on HI brain injury and study the precise mechanism of action. In this study, a mouse model of HI brain injury was established through ligating right carotid arteries. The oxygen-glucose deprivation (OGD) model was established in PC12 cells. Results showed that SNHG15 was elevated in brain tissues of mice with HI brain injury, and knockdown of SNHG15 attenuated HI-induced impairment of neurobehavioral function, brain edema, brain injury, and cell apoptosis. Besides, SNHG15 acted as a miR-153-3p sponge. SETD7 was identified to be a target of miR-153-3p. Furthermore, down-regulation of SNHG15 inhibited the OGD-induced increase in SETD7 expression in PC12 cells. Moreover, SNHG15 modulated OGD-induced cell apoptosis and decrease of cell viability through the miR-153- 3p/SETD7 axis. In conclusion, knockdown of SNHG15 alleviated HI brain injury through modulating the miR153-3p/ SETD7 axis. SNHG15 may be a prospective target for HIE therapy
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SNHG15 , miR-153-3p , SETD7 , Cell apoptosis , Hypoxic-ischemic encephalopathy , Hypoxicischemic brain injury
Citation
Histology and Histopathology Vol. 37, nº11 (2022)
URI
http://hdl.handle.net/10201/129106
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Histology and histopathology Vol.37,nº11 (2022)
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