ArticleAnnals of clinical and translational neurology2022
Upregulation of RCAN1.4 by HIF1α alleviates OGD-induced inflammatory response in astrocytes.
Article in Annals of clinical and translational neurology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 13 citations in OpenAlex.
- RNA-binding protein RCAN1.1L modulates ATF2 mRNA stability to promote mitochondrial fission in acute ischemic stroke.Cell death & disease · 2026Article
- Thermo-Magnetic Induction of Pro-Inflammatory Microglia: A Lipid-Based Nanovector Strategy for Glioblastoma Immunotherapy.ACS applied materials & interfaces · 2025Article
- Identification of plasma SEMA3E as the diagnostic biomarker for human epilepsy based on integrated bioinformatics analysis.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2025Article
- The role of astrocytes in ischemic stroke - mechanisms, functions and treatment.Frontiers in cell and developmental biology · 2025Review
- Mitochondria-related HSDL2 is a potential biomarker in temporal lobe epilepsy by modulating astrocytic lipid metabolism.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2024Article
- Astrocytes in Post-Stroke Depression: Roles in Inflammation, Neurotransmission, and Neurotrophin Signaling.Cellular and molecular neurobiology · 2023Review
- Upregulation of RCAN1.4 by HIF1α alleviates OGD-induced inflammatory response in astrocytes.Annals of clinical and translational neurology · 2022Article
- The role of circadian clock in astrocytes: From cellular functions to ischemic stroke therapeutic targets.Frontiers in neuroscience · 2022Review
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveIschemic stroke is a leading cause of human mortality and long-term disability worldwide. As one of the main forms of regulator of calcineurin 1 (RCAN1), the contribution of RCAN1.4 in diverse biological and pathological conditions has been implicated. But the role of RCAN1.4 in ischemic stroke progression remains elusive. This study is to explore the expression changes and roles of RCAN1.4 in ischemic stroke as well as the underlying mechanisms for these changes and effects of RCAN1.4 in ischemic stroke.
methodsMiddle cerebral artery occlusion model in C57BL/6J mice and oxygen-glucose deprivation (OGD) model in primary astrocytes were performed to induce the cerebral ischemic stroke. The expression pattern of RCAN1.4 was assessed using real-time quantitative PCR and western blotting in vivo and in vitro. Mechanistically, the underlying mechanism for the elevation of RCAN1.4 in the upstream was investigated. Lentiviruses were administrated, and the effect of RCAN1.4 in postischemic inflammation was clearly clarified.
resultsHere we uncovered that RCAN1.4 was dramatically increased in mouse ischemic brains and OGD-induced primary astrocytes. HIF1α, activated upon OGD, significantly upregulated RCAN1.4 gene expression through specifically binding to the RCAN1.4 promoter region and activating its promoter activity. The functional hypoxia-responsive element (HRE) was located between -254 and -245 bp in the RCAN1.4 promoter region. Moreover, elevated RCAN1.4 alleviated the release of pro-inflammatory cytokines TNFα, IL1β, IL6 and reduced expression of iNOS, COX2 in primary astrocytes upon OGD, whereas RCAN1.4 silencing has the opposite effect. Of note, RCAN1.4 overexpression inhibited OGD-induced NF-κB activation in primary astrocytes, leading to decreased degradation of IκBα and reduced nuclear translocation of NF-κB/p65.
interpretationOur results reveal a novel mechanism underscoring the upregulation of RCAN1.4 by HIF1α and the protective effect of RCAN1.4 against postischemic inflammation, suggesting its significance as a promising therapeutic target for ischemic stroke treatment.
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