ArticleJournal of molecular neuroscience : MN2020
CDKN1B Mediates Apoptosis of Neuronal Cells and Inflammation Induced by Oxyhemoglobin via miR-502-5p After Subarachnoid Hemorrhage.
Article in Journal of molecular neuroscience : MN, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 20 citations in OpenAlex.
- Cross-Platform Proteomics and Machine Learning Algorithms Nominate Plasma Biomarkers of Stroke Diagnosis.Journal of the American Heart Association · 2026Article
- Role of exercise on ncRNAs and exosomal ncRNAs in preventing neurodegenerative diseases: a narrative review.Molecular medicine (Cambridge, Mass.) · 2025Review
- The Role of miRNAs in Aneurysmal Subarachnoid Hemorrhage.Current molecular medicine · 2025Review
- Mechanism of KLF2 in young mice with pneumonia induced by Streptococcus pneumoniae.Journal of cardiothoracic surgery · 2024Article
- MiR-497-5p ameliorates the oxyhemoglobin-induced subarachnoid hemorrhage injury in vitro by targeting orthodenticle homeobox protein 1 (Otx1) to activate the Nrf2/HO-1 pathway.Molecular genetics and genomics : MGG · 2024Article
- Systemic Inflammation after Aneurysmal Subarachnoid Hemorrhage.International journal of molecular sciences · 2023Review
- The mechanism and relevant mediators associated with neuronal apoptosis and potential therapeutic targets in subarachnoid hemorrhage.Neural regeneration research · 2023Review
- Comparative transcriptomic analysis of PK15 cells infected with a PRV variant and the Bartha-K/61 vaccine strain.Frontiers in microbiology · 2023Article
- Exosome-Encapsulated microRNA-140-5p Alleviates Neuronal Injury Following Subarachnoid Hemorrhage by Regulating IGFBP5-Mediated PI3K/AKT Signaling Pathway.Molecular neurobiology · 2022Article
- The blood-brain barrier and the neurovascular unit in subarachnoid hemorrhage: molecular events and potential treatments.Fluids and barriers of the CNS · 2022Review
- MicroRNA-221-3p alleviates cell apoptosis and inflammatory response by targeting cyclin dependent kinase inhibitor 1B in chronic obstructive pulmonary disease.Bioengineered · 2021Article
- Sex-Specific MicroRNAs in Neurovascular Units in Ischemic Stroke.International journal of molecular sciences · 2021Review
- p27Cells · 2021Review
- Toll-Like Receptor Signaling Pathways: Novel Therapeutic Targets for Cerebrovascular Disorders.International journal of molecular sciences · 2021Review
- Exosome-derived miR-196b-5p facilitates intercellular interaction in infantile hemangioma via down-regulating CDKN1B.Annals of translational medicine · 2021Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Subarachnoid hemorrhage is a common disease in the neural system, which causes high fatality rate. Therefore, it is necessary to figure out inner mechanisms of factors related to this disease. RT-qPCR was applied for measuring expressions of CDKN1B and miR-502-5p and other factors of apoptosis and inflammation. Cell viabilities were detected through CCK-8. Binding conditions between miR-502-5p and CDKN1B were detected through luciferase report assay. Western blot was used for measuring levels of proteins in PPARγ/NF-κB signaling pathway. Apoptosis and inflammation of HT22 cell line, a kind of nerve cell line, were enhanced and viabilities were suppressed by oxyhemoglobin. CDKN1B expressed lower in induced HT22 cell line and overexpressed CDKN1B could promote viabilities and suppress apoptosis as well as inflammation. MiR-502-5p was the target gene of CDKN1B and enhanced apoptosis and inflammation of cells in HT22 cell line. Furthermore, miR-502-5p reversed functions of CKDN1B in induced cells through regulating proteins in PPARγ/NF-κB signaling pathway. CDKN1B was the gene that could inhibit SAH caused by apoptosis in nerve cells and inflammation by sponging miR-502-5p and regulating factors in PPARγ/NF-κB signaling pathway, suggesting it could be a factor for protecting functions of nerve cells after SAH.
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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.