ArticleHistology and histopathology2022
LncRNA SNHG15 regulates hypoxic-ischemic brain injury via miR-153-3p/SETD7 axis.
Article in Histology and histopathology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers, 1 of them a synthesis that pooled it.
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Who cites it
7 citing papers in PubMed, 1 synthesis or guideline pooled it, 7 citations in OpenAlex.
- xCT (Slc7a11) Regulation: Lessons from Cancer Research.Neurochemical research · 2026Pooled it
- The Whole Transcriptome Sequencing Profile of Serum-Derived Exosomes and Potential Pathophysiology of Age-Related Hearing Loss.Diagnostics (Basel, Switzerland) · 2026Article
- Lysine methyltransferase SETD7 in cancer: functions, molecular mechanisms and therapeutic implications.Molecular biology reports · 2025Review
- LncRNA SNHG15 acts as a ceRNA to promote breast cancer progression through the miR-153-3p/KLF5 signal axis.Journal of Cancer · 2025Article
- mir-330-5p from mesenchymal stem cell-derived exosomes targets SETD7 to reduce inflammation in rats with cerebral ischemia-reperfusion injury.Journal of molecular histology · 2024Article
- Brain microRNA profiles after exposure to heroin in rats.Experimental brain research · 2024Article
- LncRNAs and CircRNAs as Strategies against Pathological Conditions Caused by a Hypoxic/Anoxic State.Biomolecules · 2023Review
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
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 miR-153-3p/ SETD7 axis. SNHG15 may be a prospective target for HIE therapy.
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