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The effect of knocking down miR-27b on DIV14 mouse cortical neurons

ABSTRACT: To understand the effect of reducing miR-27b levels on genome-wide expression in cortical neurons and identify potential targets of miR-27b, we generated dissociated cortical neuron cultures and treated them with lentivirus to knock down miR-27b. 2 treatment conditions (control lentivirus or lentivirus to knock down miR-27b); 3 neuronal preparations of dissociated mouse cortical neurons; total of 6 samples

ORGANISM(S): Mus musculus

SUBMITTER: Vivian Poon

PROVIDER: E-GEOD-73275 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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The effect of knocking down miR-27b on DIV14 mouse cortical neurons

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Project description:Aim: The heart undergoes pathological remodelling under increased stress and neuronal imbalance. MicroRNAs (miRNAs) are involved in post-transcriptional regulation of genes in cardiac physiology and pathology. However, the mechanisms underlying miRNA-mediated regulation of pathological cardiac remodelling remain to be studied. This study aims to explore the function of endogenous microRNA-27b-3p (miR-27b-3p) in pathological cardiac remodelling. Methods and results: We found that miR-27b-3p expression was elevated in heart of patients with cardiac hypertrophy and in transverse aortic constriction (TAC)-induced cardiac hypertrophy mouse model. MiR-27b-3p-knockout mice showed significantly attenuated cardiac hypertrophy, fibrosis, and inflammation induced by two independent pathological cardiac hypertrophy models, TAC and Angiotensin II (Ang II) perfusion. Transcriptome sequencing analysis revealed that miR-27b-3p deletion significantly downregulated TAC-induced cardiac hypertrophy, fibrosis, and inflammatory genes. We identified fibroblast growth factor 1 (FGF1) as a novel miR-27b-3p target gene in the heart, which was upregulated in miR-27b-3p-null mice. Conclusions: Our study has demonstrated that miR-27b-3p induces pathological cardiac remodelling and suggests that inhibition of endogenous miR-27b-3p or administration of FGF1 might have the potential to suppress cardiac remodelling in a clinical setting.

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