LncRNA XIST knockdown attenuates Aβ25-35-induced toxicity, oxidative stress, and apoptosis in primary cultured rat hippocampal neurons by targeting miR-132.

Alzheimer's disease (AD) is a progressive and irreversible neurodegenerative disorder. The abnormal accumulation and deposition of amyloid-beta peptide (Aβ) in senile plaques and cerebral vasculature is widely recognized to be the most likely culprit in the pathogenesis of AD. Long non-coding RNAs (lncRNAs), a kind of evolutionarily conserved non-coding RNAs with over 200 nucleotides in length, have introduced a novel field of biology, and are involved in various human diseases, including neurological diseases. Recently, lncRNA X-inactive specific transcript (XIST) is reported to be upregulated in the rat spinal cord injury (a neurological disease) model and XIST knockdown has a prominent protective effect on the recovery of spinal cord injury. However, little is known about the expression and function of XIST in AD. Here, we showed that Aβ25-35 treatment increased XIST expression in hippocampal neurons. XIST knockdown ameliorated toxicity, oxidative stress, and apoptosis induced by Aβ25-35 treatment in hippocampal neurons. We further identified and confirmed that miR-132 was the target of XIST, and XIST functioned by targeting miR-132. Collectively, these data show that knockdown of XIST relieves Aβ25-35-induced toxicity, oxidative stress, and apoptosis in primary cultured rat hippocampal neurons by upregulation of miR-132. These findings encourage continued investigation of the potential of manipulating XIST in the treatment of AD. IJCEP