Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P10415 (Bcl-2)
 33,771 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Emerging evidence has unraveled the important implications of microRNAs (miRNAs/miRs) in intracerebral hemorrhage (ICH). The aim of the present study was to assess the possible regulatory role of miR-26a-5p in ICH both in vivo and in vitro. ICH model of rats was constructed using stereotactic injection of VII collagenase, and ICH condition of PC-12 cells was stimulated by hemin. Exogenous overexpression of miR-26a-5p was achieved utilizing the transfection with miR-26a-5p agomir or miR-26a-5p mimics. We detected decreased miR-26a-5p and increased RAN binding protein 9 (RANBP9) levels in perihematomal tissues of ICH rats and in PC-12 cells following ICH. While miR-26a-5p overexpression alleviated behavioral deficits and neuronal apoptosis of rats with ICH. Apoptosis-related proteins Bax, Bcl-2 and cleaved caspase-3 in perihematomal region were also measured to further confirm the inhibitory effect of miR-26a-5p on neuronal apoptosis. In ICH models in vitro, we found that miR-26a-5p overexpression significantly decreased hemin-stimulated apoptosis of PC-12 cells. Additionally, RANBP9 knockdown could suppress the apoptosis of PC-12 cells, similar to the effects of PC-12 cells transfected with miR-26a-5p mimics. With dual-luciferase reporter assay, we identified that miR-26a-5p directly targeted RANBP9. In conclusion, exogenous miR-26a-5p alleviated neuronal apoptosis and brain injury partially by targeting RANBP9, and miR-26a-5p/RANBP9 axis may be a potential target for ICH treatment.
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PMID:MicroRNA-26a-5p alleviates neuronal apoptosis and brain injury in intracerebral hemorrhage by targeting RAN binding protein 9. 3262 24