The alternative 3′ splice site of <i>GPNMB</i> may promote neuronal survival after neonatal hypoxic–ischemic encephalopathy injury

This study aimed to decipher the effect of glycoprotein nonmetastatic melanoma protein B (GPNMB) on neonatal hypoxic–ischemic encephalopathy (NHIE) and its potential molecular mechanism. The (HI) model was established in 7-day-old rats, then, Zea-Longa scores Nissl staining were performed measure brain damage post-HI. In addition, gene sequencing used detect differential expression genes (DEGs), Gene Ontology Kyoto Encyclopedia Genes Genomes databases determine function DEGs. Furthermore, an oxygen–glucose deprivation (OGD) developed SY5Y cells human fetal neurons, level GPNMB verified by quantitative real-time polymerase chain reaction. methyl thiazolyl tetrazolium cell counting kit-8 assays applied after interference. Finally, alternative splicing analyzed using Splice Grapher software. results indicated that HI induced marked neurological impairment neuron injury rats. Also, most obviously upregulated Additionally, significantly neurons OGD, GPNMB-si promoted increase viability number. Moreover, we found type Alternative 3′ splice site, with site 143382985:143404102. Herein, promotes a crucial regulatory mechanism for neuronal survival NHIE.