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MicroRNA-124 conducts neuroprotective effect via inhibiting AK4/ATF3 after subarachnoid hemorrhage
Wei Jiang1, Qingge Jia2, Hongxin Ma1
1Department of Neurosurgery, General Hospital of Northern Theater Command, Wenhua Rd. No.83, Shenyang, 110000, Liaoning, China.
Abstract:
Spontaneous subarachnoid hemorrhage (SAH) accounts for approximately 5% of all cases of stroke. SAH is correlated with elevated rates of mortality and disability. Despite significant advancements in comprehending the pathogenesis and surgical management, efficacious clinical interventions remain restricted, and the prognosis is yet to be enhanced. MicroRNAs play a crucial role in various pathological processes in organisms. Revealing these regulatory processes is conducive to the development of new treatment methods. MicroRNA-124 is highly expressed in the nervous system and has significant research value for SAH. This study aims to explore the role of miR-124 in the early post-SAH period on neural function and verify whether it is involved in the pathological and physiological processes of SAH. In this study, we used methods such as comparing the expression levels of miR-124 in cerebrospinal fluid, establishing a rat SAH model, and a mouse embryonic primary neuron hemoglobin stimulation model to verify the downstream proteins of miR-124 in SAH. Through transfection techniques, we adjusted the expression of this small RNA in Vitro and in Vivo models using miR-124 inhibitor and mimic in the primary neuron hemoglobin stimulation model and rat SAH model, and observed the phenotype. Finally, by consulting the literature and verifying in Vivo and in Vitro methods, AK4 and downstream molecule ATF3 were identified as downstream targets of miR-124.
Insights
MicroRNA-124 plays a key role in early brain injury following spontaneous subarachnoid hemorrhage (SAH). Targeting miR-124 may offer new therapeutic strategies for improving outcomes after SAH.
Area of Science:
- Neuroscience
- Molecular Biology
- Genetics
Background:
- Spontaneous subarachnoid hemorrhage (SAH) is a severe stroke type with high mortality and disability rates.
- Current treatments for SAH are limited, necessitating novel therapeutic targets.
- MicroRNAs are critical regulators of cellular processes and hold potential for new SAH interventions.
Purpose of the Study:
- To investigate the role of microRNA-124 (miR-124) in early neural function after SAH.
- To determine if miR-124 is involved in the pathological and physiological mechanisms of SAH.
- To identify downstream targets of miR-124 in the context of SAH.
Main Methods:
- Compared miR-124 expression levels in cerebrospinal fluid.
- Established rat SAH and mouse primary neuron hemoglobin stimulation models.
- Utilized miR-124 inhibitors and mimics in vitro and in vivo to modulate expression and observe effects.
- Identified downstream targets using literature review and experimental verification.
Main Results:
- miR-124 expression was analyzed in relation to SAH.
- The study successfully modulated miR-124 levels in both in vitro and in vivo models.
- AK4 and ATF3 were identified as direct downstream targets of miR-124 in SAH.
Conclusions:
- miR-124 is implicated in the early stages of neural dysfunction following SAH.
- The findings suggest miR-124, through its regulation of AK4 and ATF3, is a potential therapeutic target for SAH.
- Further research into miR-124 modulation could lead to improved clinical interventions for SAH patients.
