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AhR/miR-23a-3p/PKCα axis contributes to memory deficits in ovariectomized and normal aging female mice

Shuai Zhang, Xiaobin An, Siyu Huang, Lu Zeng, Yi Xu, Dan Su, Yang Qu, Xin Tang, Jing Ma, Junkai Yang, Jing Ai

2021Molecular Therapy — Nucleic Acids21 citationsDOIOpen Access PDF

Abstract

, adeno-associated virus-mediated overexpression of miR-23a-3p (AAV-pre-miR-23a-3p) suppressed hippocampal PKCα and impaired the memory of mice. Chromatin immunoprecipitation analysis showed that aryl hydrocarbon receptor (AhR) binds the promoter region of miR-23a-3p. The AhR-dependent downregulation of PKCα could be prevented by AMO-23a as well. Furthermore, knockdown of miR-23a-3p using AAV-AMO-23a rescued the cognitive and electrophysiological impairments of OVX and normal aging female mice. We conclude that long-term estrogen deficiency impairs cognition and hippocampal LTP by activating the AhR/miR-23a-3p/PKCα axis. The knockdown of miR-23a-3p may be a potentially valuable therapeutic strategy for estrogen deficiency-induced memory deficits.

Topics & Concepts

Hippocampal formationLong-term potentiationHippocampusEndocrinologyGene knockdownDownregulation and upregulationInternal medicineOvariectomized ratEstrogenMemory impairmentChromatin immunoprecipitationBiologyMedicineChemistryNeuroscienceReceptorCognitionPromoterBiochemistryGene expressionApoptosisGeneEstrogen and related hormone effectsMicroRNA in disease regulationCancer-related cognitive impairment studies