LncRNA SNHG14 promoted inflammation of cerebral apoplexy by miR-124-3p/TRAF6 axis

Li, Fang

doi:10.1007/s13273-021-00197-8

Cited by 1 publication

(2 citation statements)

References 23 publications

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“…LncRNA SNHG14 induces inflammation in an in vitro stroke model by inhibiting the miR-124-3p/TRAF6 axis. In addition, down-regulation of LncRNA SNHG14 attenuated inflammation in an in vitro stroke model by inducing the miR-124-3p/TRAF6 axis (217). Bu et al (2021) found that silencing SNHG14 could significantly promote OGD-induced primary cortical neuron proliferation, inhibit apoptosis and inflammatory responses, and alleviate neuronal damage.…”

Section: Mechanism Of Nkila Involved In Stroke Neuroinflammationmentioning

confidence: 99%

“…High expression of SNHG14 increases the expression of lipoprotein-related phospholipase by inhibiting miR-145-5p, which promotes the release of a large number of inflammatory cytokines (TNF-a, NO) after ischemia and aggravates neuronal damage (31). Li (2022) found that LncRNA SNHG14 was highly expressed in stroke patients. LncRNA SNHG14 induces inflammation in an in vitro stroke model by inhibiting the miR-124-3p/TRAF6 axis.…”

Section: Mechanism Of Nkila Involved In Stroke Neuroinflammationmentioning

confidence: 99%

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A systematic review of the research progress of non-coding RNA in neuroinflammation and immune regulation in cerebral infarction/ischemia-reperfusion injury

Yang

Zeng

et al. 2022

Front. Immunol.

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Cerebral infarction/ischemia-reperfusion injury is currently the disease with the highest mortality and disability rate of cardiovascular disease. Current studies have shown that nerve cells die of ischemia several hours after ischemic stroke, which activates the innate immune response in the brain, promotes the production of neurotoxic substances such as inflammatory cytokines, chemokines, reactive oxygen species and − nitrogen oxide, and mediates the destruction of blood-brain barrier and the occurrence of a series of inflammatory cascade reactions. Meanwhile, the expression of adhesion molecules in cerebral vascular endothelial cells increased, and immune inflammatory cells such as polymorphonuclear neutrophils, lymphocytes and mononuclear macrophages passed through vascular endothelial cells and entered the brain tissue. These cells recognize antigens exposed by the central nervous system in the brain, activate adaptive immune responses, and further mediate secondary neuronal damage, aggravating neurological deficits. In order to reduce the above-mentioned damage, the body induces peripheral immunosuppressive responses through negative feedback, which increases the incidence of post-stroke infection. This process is accompanied by changes in the immune status of the ischemic brain tissue in local and systemic systems. A growing number of studies implicate noncoding RNAs (ncRNAs) as novel epigenetic regulatory elements in the dysfunction of various cell subsets in the neurovascular unit after cerebral infarction/ischemia-reperfusion injury. In particular, recent studies have revealed advances in ncRNA biology that greatly expand the understanding of epigenetic regulation of immune responses and inflammation after cerebral infarction/ischemia-reperfusion injury. Identification of aberrant expression patterns and associated biological effects of ncRNAs in patients revealed their potential as novel biomarkers and therapeutic targets for cerebral infarction/ischemia-reperfusion injury. Therefore, this review systematically presents recent studies on the involvement of ncRNAs in cerebral infarction/ischemia-reperfusion injury and neuroimmune inflammatory cascades, and elucidates the functions and mechanisms of cerebral infarction/ischemia-reperfusion-related ncRNAs, providing new opportunities for the discovery of disease biomarkers and targeted therapy. Furthermore, this review introduces clustered regularly interspaced short palindromic repeats (CRISPR)-Display as a possible transformative tool for studying lncRNAs. In the future, ncRNA is expected to be used as a target for diagnosing cerebral infarction/ischemia-reperfusion injury, judging its prognosis and treatment, thereby significantly improving the prognosis of patients.

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Section: Mechanism Of Nkila Involved In Stroke Neuroinflammationmentioning

confidence: 99%

Section: Mechanism Of Nkila Involved In Stroke Neuroinflammationmentioning

confidence: 99%