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Preparation of Acute Hippocampal Slices from Rats and Transgenic Mice for the Study of Synaptic Alterations during Aging and Amyloid Pathology
Published on: March 23, 2011
IGF2BP2-Shox2 axis regulates hippocampal-neuronal senescence to alleviate microgravity-induced recognition
Yujie Zhao1,2, Guohua Ji1, Sihai Zhou1,2
1State Key Laboratory of Space Medicine, China Astronaut Research and Training Center, Beijing, China.
Abstract:
During space travel, microgravity leads to disturbances in cognitive function, while the underlying mechanism is still unclear. Simulated microgravity mice showed neuronal age-like changes in the hippocampus of our study. In the context of microgravity, we discovered m6A modification reshapes in the hippocampal region. When paired with RNA-seq and MeRIP-seq, Shox2 was found to be a powerful regulator in hippocampal neuron that respondes to microgravity. Decreased expression of senescence-associated secretory phenotype factors and improved genes related to synapses led to the restoration of memory function in the hippocampus upon increased expression of Shox2. Moreover, we discovered that IGF2BP2 was required for the m6A modification of the Shox2, and overexpressed IGF2BP2 in the hippocampus protected against both neuronal senescence and learning and memory decline caused by loss of gravity. Accordingly, our research identified the hippocampal IGF2BP2-Shox2 axis as a possible therapeutic approach to maintaining cognitive function during space travel.
Insights
Space travel impairs cognitive function. This study reveals the IGF2BP2-Shox2 pathway in the hippocampus mitigates microgravity-induced memory decline and neuronal aging.
Area of Science:
- Neuroscience
- Space Biology
- Molecular Biology
Background:
- Microgravity during space travel causes cognitive deficits, but mechanisms remain unknown.
- Neuronal aging-like changes occur in the hippocampus under simulated microgravity.
- RNA modifications, specifically m6A, are altered in the hippocampus during microgravity exposure.
Purpose of the Study:
- To investigate the molecular mechanisms underlying cognitive dysfunction in microgravity.
- To identify key regulators of hippocampal neuronal response to microgravity.
- To explore potential therapeutic targets for preserving cognitive function during space travel.
Main Methods:
- Simulated microgravity models in mice.
- RNA sequencing (RNA-seq) and m6A-specific immunoprecipitation sequencing (MeRIP-seq).
- Analysis of gene expression, senescence markers, and synaptic gene regulation.
Main Results:
- Shox2 was identified as a critical regulator of hippocampal neurons responding to microgravity.
- Increased Shox2 expression reversed microgravity-induced cognitive decline by reducing senescence factors and enhancing synaptic genes.
- IGF2BP2 was essential for Shox2 m6A modification and protected against neuronal senescence and memory impairment.
Conclusions:
- The hippocampal IGF2BP2-Shox2 axis is a key player in mitigating microgravity-induced cognitive decline.
- Targeting the IGF2BP2-Shox2 pathway may offer a therapeutic strategy for maintaining cognitive function during space missions.
- This research provides insights into the molecular basis of space travel's impact on the brain.
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