Background: Evidence has shown that microRNAs (miRNAs) are implicated in ischemic diseases. Therefore, the aim of the present study was to identify the functions of astrocyte (ATC)-derived exosomal miR-361 on cerebral ischemic-reperfusion (I/R) injury. Methods: A rat model of cerebral I/R injury was initially established, followed by injection of ATC-derived exosomes. Next, the protective function of ATC-derived exosomes in rats with cerebral I/R injury was evaluated, and then the effect of miR-361 on rats with cerebral I/R injury was evaluated by changing miR-361 expression in exosomes. PC12 cells that underwent oxygenglucose deprivation/reoxygenation were used to simulate I/R in vitro. The effect of ATC-derived exosomal miR-361 on the viability and apoptosis of OGD/R-treated PC12 cells was also assessed. The bioinformatic analysis predicted the targeted gene of miR-361. Results: It was found that I/R was damaging to the brain nerves of rats, while ATC-derived exosomal miR-361 relieved nerve damage caused by I/R. Furthermore, the in vitro experiments demonstrated that ATC-derived exosomal miR-361 increased OGD/R-inhibited PC12 cell activity and suppressed cell apoptosis. Bioinformatics predicted that miR-361 targeted cathepsin B (CTSB). CTSB upregulation blocked the protective roles of miR-361. In addition, miR-361 was found to downregulate the AMPK/mTOR signaling pathway by targeting CTSB. Conclusion: The present study demonstrated that ATC-derived exosomal miR-361 alleviates nerve damage in rats with cerebral I/R injury by targeting CTSB and downregulating the AMPK/mTOR pathway. This may offer novel insights into treatment for I/R injury.
Neural stem cell (NSC) transplantation is one of the most promising therapeutic strategies for neurodegenerative diseases. However, the slow spontaneous differentiation of NSCs often hampers their application in neural repair. Although some biological growth factors accelerate the differentiation of NSCs, their high cost, short half‐life, and unpredictable behavior in vivo, as well as the complexity of the operation, hinder their clinical use. In this study, it is demonstrated that hydroxyapatite (HAp), the main component of bone, in the form of nanorods, can regulate the neural differentiation of NSCs and maturation of the newly differentiated cells. Culturing NSCs with HAp nanorods leads to the differentiation of NSCs into mature neurons that exhibit well‐defined electrophysiological behavior within 5 days. The state of these neurons is much better than when culturing the cells without HAp nanorods, which undergo a 2‐week differentiation process. Furthermore, RNA‐sequencing data reveal that the neuroactive ligand–receptor interaction pathway is dominant in the enriched differentiated neuronal population. Hence, inorganic growth factors like HAp act as a feasible, effective, safe, and practical tool for regulating the differentiation of NSCs and can potentially be used in the treatment of neurodegenerative diseases.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.