Evidence map›Paper›PMID 37716929›Full record

ArticleExperimental brain research2023

CircNCOA4 knockdown attenuates OGD-induced neuron injury through miR-338-5p/PDE4B axis.

Danyang Wang, Sai Xiao, Xiaoming Li, Wenbo Qi

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Article in Experimental brain research, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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4 authors.

Danyang WangDepartment of Clinical Laboratory, Qingdao Mental Health Center, Qingdao, 266000, China.
Sai XiaoDepartment of Geriatrics, Qingdao Mental Health Center, Qingdao, 266000, China.
Xiaoming LiDepartment of Pharmacy, Qingdao Mental Health Center, Qingdao, 266000, China.
Wenbo QiQuality Management Division, Qingdao Mental Health Center, No. 299, Nanjing Road, North District, Qingdao, 266000, China. qwb_101@163.com.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Circular RNAs (circRNAs) have been revealed to be involved in the pathology of acute ischemic stroke (AIS). Herein, we aimed to study the role and mechanism of circNCOA4 in ischemic stroke. The neuron-like cell line SK-N-SH of the experiment group was cultured in oxygen-glucose deprivation (OGD) condition. Cell viability and apoptosis were evaluated by cell counting kit-8 and flow cytometry. The oxidative damage and endoplasmic reticulum stress (ERS) were analyzed by measuring the production of reactive oxygen species (ROS), malondialdehyde (MDA), superoxide dismutase (SOD), and ERS-related markers. The binding between miR-338-5p and circNCOA4 or PDE4B (Phosphodiesterase 4B) was confirmed using dual-luciferase reporter and RIP assays. The commercial kit was used for exosome separation. The levels of circNCOA4 and PDE4B were increased, while miR-338-5p expression was decreased by OGD stimulation. OGD stimulation resulted in the apoptosis of neurons and induced oxidative damage and ERS, these effects were attenuated by circNCOA4 knockdown, while reinforced by circNCOA4 overexpression. Mechanistically, circNCOA4 acted as a sponge for miR-338-5p, and PDE4B was a target of miR-338-5p. MiR-338-5p inhibition reversed the neuroprotective effects of circNCOA4 silencing on neurons. Besides, miR-338-5p overexpression could abolish OGD-induced neuron injury, which was reversed by PDE4B upregulation. In addition, circNCOA4 was packaged into exosomes and showed potential diagnostic value for acute ischemic stroke (AIS) patients. CircNCOA4 has potential diagnostic value for AIS patients and promoted OGD-induced neuron injury via the miR-338-5p/PDE4B axis, providing a new insight into the pathology of AIS.

Indexed as

Ischemic StrokeMicroRNAsApoptosisCyclic Nucleotide Phosphodiesterases, Type 4GlucoseHumansCyclic Nucleotide Phosphodiesterases, Type 4GlucoseMicroRNAsMIRN338 microRNA, humanPDE4B protein, humanAcute ischemic strokecircNCOA4miR-338-5pPDE4B

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.