Neuroscience
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Neonatal hypoxia-ischemia encephalopathy (HIE) is a significant reason for neonatal mortality and prolonged disability. We have previously revealed that GPR39 activation attenuates neuroinflammation in a neonatal HIE rat model. This study aimed to investigate whether GPR39 affected microglial pyroptosis post-HIE. ⋯ METTL3 inhibits microglial pyroptosis in neonatal HIE via regulating m6A-HuR dependent stabilization of GPR39, which contributes to therapeutics development for neonatal HIE.
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This review explores the significant roles of neurotransmitters, focusing on dopamine and serotonin, in inflammation and cancer. These neurotransmitters are vital for neural signaling and play crucial roles in various physiological and pathological processes. ⋯ The interplay between dopamine and serotonin systems extends beyond neural communication, significantly affecting immune responses and inflammation. Dopamine's role in modulating immune cell activity highlights its potential in treating inflammatory conditions and cancer. Similarly, serotonin's extensive physiological impact underscores the importance of targeting 5-HT pathways in various disorders. Future research should focus on developing therapeutic strategies that leverage these neurotransmitters' regulatory functions in both the CNS and peripheral systems.
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Stem-cell derived extracellular vesicles (EVs) have shown promise in preclinical spinal cord injury (SCI) models but lack a comprehensive literature review for clinical translation guidance. ⋯ Both natural and bio-engineered EVs improve functional and pathological outcomes in animal models of SCI. The enhanced benefits observed with bio-engineered EVs, particularly those utilizing surface modification approaches, highlight the importance of continued exploration into bio-engineering techniques to optimize EVs' therapeutic efficacy for SCI repair. Protocol Registration CRD42024512122.
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The study aimed to validate the protective effect of neuroglobin (Ngb) in a cell model of Parkinson's disease (PD) and explore its therapeutic potential. Lentivirus-Ngb (LvNgb) and siRNA-Ngb (siNgb) were used to achieve Ngb overexpression and knockdown, respectively, in a sporadic PD cell model. Apoptosis was evaluated by flow cytometry-based Annexin V/propidium iodide assays. ⋯ Furthermore, Ngb overexpression restored MMP and NAD+/NADH ratios and alleviated ROS-mediated oxidative stress in MN9D cells. Finally, Co-IP confirmed the interaction between Ngb and NDUFA10 in MN9D cells. In conclusion, Ngb protects MN9D cells against apoptosis by interacting with Complex I subunit NDUFA10, rescuing its activity and inhibiting the mitochondrial pathway of apoptosis in the MPP+-mediated PD model.
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Degenerative diseases and injuries of central nervous system (CNS) often cause nerve cell apoptosis and neural dysfunction. Protection of surviving cells or inducing the differentiation of stem cells into functional cells is considered to be an important way of neurorepair. In addition, transdifferentiation technology emerged recently is expected to provide new solutions for nerve regeneration. ⋯ The extracellular microenvironment changed dramatically upon neural lesion, exploring the biological function of signals mediated by cell surface receptors will help to develop molecular strategies for nerve regeneration. An increasing number of studies have reported that cell surface receptor-mediated signaling affects the survival, differentiation, and functioning of neural cells, and even regulate their trans-lineage reprogramming. Here, we provide a review on the roles of cell surface receptors in CNS regeneration, thus providing new cues for better treatment of neurodegenerative diseases or nerve injury.