Home General Physiology and Biophysics 2025 General Physiology and Biophysics Vol.44, No.4, p. 337–348, 2025

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Founded: 1982
ISSN 1338-4325 (online)
ISSN 0231-5882 (print)
Published in English,
6 times per year

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General Physiology and Biophysics Vol.44, No.4, p. 337–348, 2025

Title: Exosomal microRNA-22-3p influences oxidative stress injury and neuronal apoptosis in Alzheimer’s disease via targeting KDM6B
Author: Luzy Zhang
Abstract: This research was intended to unravel the effects of exosomal microRNA-22-3p (miR-22-3p) secreted from bone marrow mesenchymal stem cells (BMSCs) on oxidative stress damage and neuronal apoptosis in Alzheimer’s disease (AD) via KDM6B. BMSCs and BMSCs-derived exosomes (BMSCs-Exos) were obtained and identified. An in vitro AD model was established. The levels of miR-22-3p and KDM6B were tested. Cell viability, ROS levels, MDA content and SOD levels, as well as apoptosis levels, were evaluated. The targeting relationship between miR-22-3p and KDM6B was validated. BMSC-Exos, miR-22-3p mimic and KDM6B siRNA advanced the cell viability, attenuated cell apoptosis, and ameliorated the oxidative stress injury of Aβ1-42-induced HT22 cells, including the decrease in the content of ROS and MDA and the increase in SOD activity. miR-22-3p inhibitor and KDM6B overexpression lentivirus advanced the decrease of cell viability, aggravated cell apoptosis, and promoted oxidative stress injury in Aβ1-42-induced HT22 cells, including the increase of ROS and MDA content and the decrease of SOD activity. miR-22-3p mimic combined with oe-KDM6B reversed the effects caused by miR-22-3p mimic alone. miR-22-3p targeted KDM6B. BMSC-Exos-derived miR-22-3p suppresses KDM6B expression to alleviate oxidative stress damage and apoptosis in AD neurons.
Keywords: Alzheimer’s disease — MicroRNA-22-3p — Lysine-specific demethylase 6B — BMSCs — Exosome — Oxidative stress — Neuronal apoptosis
Year: 2025, Volume: 44, Issue: 4 Page From: 337, Page To: 348
doi:10.4149/gpb_2025009


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