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Integrative analysis of microRNA-mediated mitochondrial dysfunction in hippocampal neural progenitor cell death within cognitive deficit models
Seong Who Kim 3,4,5,*,# (Professor), Ha-Na Woo 3,5,# (Research professor), A Reum Han1,3,4 (Graduate student), Tae Kwon Moon2 (Graduate student), Im Kyeung Kang2 (Graduate student), Dae Bong Yu 2 (Graduate student), Yechan Kim2 (College student), Cheolhwan Byon2 (College student), Sujeong Park 2 (Research worker), Hae Lin Kim2 (Research worker), Kyoung Jin Lee2,5 (Research professor), Heuiran Lee 2,5 (Professor)
1Translational Medicine and 2Microbiology and 3Biochemistry and Molecular Biology, Asan Medical Institute of Convergence Science and Technology, Asan Medical Center, University of Ulsan College of Medicine,
4Stem Cell Immunomodulation Research Center and 5Bio-Medical Institute of Technology, University of Ulsan College of Medicine
Abstract
Adult hippocampal neurogenesis plays a pivotal role in maintaining cognitive brain function; however, this process diminishes with age, particularly in patients with neurodegenerative disorders. While small, non-coding microRNAs (miRNAs) are crucial for hippocampal neural stem (HCN) cell maintenance, their involvement in neurodegenerative disorders remains unclear. This study aims to elucidate the mechanisms through which miRNAs regulate HCN cell death and their potential involvement in neurodegenerative disorder. We performed a comprehensive microarray-based analysis to investigate changes in miRNA expression in insulin-deprived HCN cells, as an in vitro model for cognitive impairment. Remarkably, miR-150-3p, miR-323-5p, and miR-370-3p which increased significantly over time following insulin withdrawal, induced pronounced mitochondrial fission and dysfunction, ultimately leading to HCN cell death. Notably, these miRNAs collectively target the mitochondrial fusion protein OPA1, with miR-150-3p also targeting MFN2. Furthermore, data-driven analyses involving human subjects within the hippocampus and brain revealed significant reductions of OPA1 and MFN2 in the Alzheimer's disease (AD) patients. Our results indicate that miR-150-3p, miR-323-5p, and miR-370-3p contribute to deficits in hippocampal neurogenesis by modulating mitochondrial dynamics. Our findings provide a novel insight into the intricate connection between miRNAs and mitochondrial dynamics, shedding light on their potential involvement in conditions characterized by deficits in hippocampal neurogenesis, such as AD.
Abstract, Accepted Manuscript [Submitted on September 8, 2023, Accepted on November 28, 2023]
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