Long Noncoding RNA X-Inactive Specific Transcript Regulates Neuronal Cell Apoptosis in Ischemic Stroke Through...

Area of Science:

• Neuroscience
• Molecular Biology
• Genetics

Background:

• Long noncoding RNA X-inactive specific transcript (XIST) is implicated in neurodegenerative disorders.
• The specific role and regulatory mechanisms of XIST in ischemic stroke are not well understood.

Purpose of the Study:

• To investigate the expression and function of XIST in ischemic stroke.
• To elucidate the molecular mechanism underlying XIST's role in ischemic stroke, focusing on the miR-98/BACH1 axis.

Main Methods:

• XIST expression analysis in mice with middle cerebral artery occlusion and oxygen-glucose deprivation (OGD)-treated neurons.
• Functional assays to assess cell viability, apoptosis, and caspase-3 activity following XIST interference.
• Interaction studies between XIST, miR-98, and BTB-to-CNC homology 1 (BACH1).

Main Results:

• XIST expression was significantly upregulated in both in vivo and in vitro models of ischemic stroke.
• XIST knockdown enhanced neuronal viability and reduced apoptosis and caspase-3 activity in OGD-treated neurons.
• XIST interacted with miR-98, which targets BACH1. Silencing miR-98 or overexpressing BACH1 reversed the neuroprotective effects of XIST knockdown.

Conclusions:

• XIST promotes the progression of ischemic stroke by regulating the miR-98/BACH1 axis.
• Targeting the XIST/miR-98/BACH1 pathway presents a potential novel therapeutic strategy for ischemic stroke treatment.