Journal
BRAIN RESEARCH BULLETIN
Volume 176, Issue -, Pages 43-53Publisher
PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.brainresbull.2021.08.003
Keywords
Ischemic stroke; LncRNA HOTAIR; microRNA-148a-3p; KLF6; Neurological function recovery; STAT3 signaling pathway; Apoptosis; Inflammation
Categories
Funding
- GuangzhouScience and Technology Planning Project [2060404]
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In this study, it was found that post-ischemic stroke, HOTAIR absorbed miR-148a3p and upregulated KLF6 expression, promoting apoptosis and inflammation, exacerbating neurological injury.
Ischemic stroke (IS), caused by a permanent or transient local reduction in blood supply to the brain, is one of the most widespread causes of public health problems in modern society. Long non-coding RNA (LncRNA) has been reported to be related to angiogenesis following IS. In this study, we explored the effect and potential molecular mechanism of lncRNA homeobox antisense non-coding RNA (HOTAIR) in IS. Permanent middle cerebral artery occlusion (pMCAO) model and oxygen and glucose deprivation (OGD) model were established. HOTAIR was increased in vivo and in vitro models post-ischemic. HOTAIR knockdown promoted neurological function recovery, manifesting in decreased modified neurological severity score, cerebral infarcted area, apoptosis and inflammation, and improved balance ability, spatial learning and memory ability. Silencing HOTAIR also improved the viability of OGD-induced N2a cells, and attenuated apoptosis and inflammation. HOTAIR can compete with KLF6 to bind to miR-148a-3p. miR-148a-3p knockdown or KLF6 overexpression partially reversed the effect of sh-HOTAIR on OGD-induced N2a cells. HOTAIR suppressed the activation of STAT3 pathway via the miR-148a-3p/KLF6 axis. To summarize, this study demonstrated that lncRNA HOTAIR absorbed miR-148a3p and up-regulated KLF6 expression through ceRNA mechanism, and inhibited STAT3 pathway, promoted apoptosis and inflammation, and aggravated neurological injury post-IS.
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