MicroRNA-132-3p alleviates neuron apoptosis and impairments of learning and memory abilities in Alzheimer’s disease by downregulation of HNRNPU stabilized BACE1

Qu, Jie; Xiong, Xiaowei; Hujie, Gulibaha; Yan, Long; Ma, Liqun

doi:10.1080/15384101.2021.1982507

Cited by 20 publications

(19 citation statements)

References 37 publications

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“…HNRNPU knockdown reduced the mRNA and protein expression levels of ZBTB7A and mRNA expression levels of RP11-386G11.10 ( Figure 8 F–G). As reported, HNRNPU promotes cancer progression by stabilizing downstream target gene mRNA [ [29] , [30] , [31] , [32] ], and we observed that the stability of ZBTB7A mRNA decreases after HNRNPU knockdown in HCC cells as expected ( Figure 8 H). In addition, HNRNPU overexpression increased the relative luciferase activity of RP11-386G11.10-WT cells ( Figure 8 I).…”

Section: Resultssupporting

confidence: 87%

A novel lncRNA RP11-386G11.10 reprograms lipid metabolism to promote hepatocellular carcinoma progression

Xia

Gongye

et al. 2022

Molecular Metabolism

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Section: Resultssupporting

confidence: 87%

A novel lncRNA RP11-386G11.10 reprograms lipid metabolism to promote hepatocellular carcinoma progression

Xia

Gongye

et al. 2022

Molecular Metabolism

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“…We demonstrated that the activated microglial cells caused by miR-132-3p leads to increased cell apoptotic rate and diminished viability of neuroblastoma cells. However, miR-132-3p was also reported to alleviate neuron apoptosis and impairments of learning and memory abilities in Alzheimer's disease (Qu, Xiong, Hujie et al, 2021). Alzheimer's disease and PD, both belonging to neuro-degenerative disease, the former is a neurodegenerative brain pathology formed due to piling up of amyloid proteins, development of plaques and disappearance of neurons (Tufail, Ma, Zhang et al, 2021).while the latter is caused by the loss of dopaminergic neurons in the substantia nigra (Xu, Zhang, Kang et al, 2021).…”

Section: Discussionmentioning

confidence: 99%

Mechanism of miR-132-3p Promoting Neuroinflammation and Dopaminergic Neurodegeneration in Parkinson’s Disease

Gong

Huang

Chen

2022

eNeuro

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The major pathology in Parkinson's disease (PD) is neuron injury induced by degeneration of dopaminergic neurons and the activation of microglial cells. The objective of this study is to determine the effect and mechanism of miR-132-3p in regulating neuroinflammation and the degeneration of dopaminergic neuron in PD.The expressions of miR-132-3p in brain tissues of PD patients, LPS induced BV-2 cells and MPTP induced PD mouse models were detected. The effect of miR-132-3p and GLRX in cell viability, apoptosis and inflammation was verified in BV-2 cells.The activation of Iba1 in substantia nigra pars compacta and the loss of tyrosine hydroxylase were detected in PD mouse models and the mobility of mouse models was assessed as well. The targeting relationship between miR-132-3p and GLRX was confirmed by RIP and dual luciferase reporter gene assay. Elevated expression of miR-132-3p and decreased expression of GLRX were found in PD patients and cells models. Overexpression of miR-132-3p can induce activation of microglial cells, which can be reversed by GLRX overexpression. Collected evidence in both cell model and mouse models showed the effect of miR-132-3p in enhancing the activation of microglial cells and the loss of microglia cells, which was achieved by mediating GLRX.

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“…RBPs have been recognized as a crucial player in AD development [ 40 ]. For example, overexpression of RBP-HNRNPU bound to BACE1 mRNA to regulate the stability of BACE1 mRNA hence resulted in learning and memory abilities impairment in AD rat [ 41 ]. Our study revealed that RBP-TARBP2 significantly elevated in Aβ(1–42)-incubated ECs and participated in BBB permeability regulation.…”

Section: Discussionmentioning

confidence: 99%

TARBP2-stablized SNHG7 regulates blood-brain barrier permeability by acting as a competing endogenous RNA to miR-17-5p/NFATC3 in Aβ-microenvironment

et al. 2022

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Breakdown of blood-brain barrier (BBB) is recognized as serious pathological marker of Alzheimer’s disease development. Studies confirmed that β-amyloid (Aβ) deposition induced high BBB permeability by disrupting tight junction (TJ) proteins formed from endothelial cells (ECs). Here, we found TARBP2, SNHG7 and NFATC3 in expressions were increased and miR-17-5p expression was decreased in Aβ(1-42)-incubated ECs. Overexpression of TARBP2, SNHG7 and NFATC3 elevated BBB permeability and knockdown of them had converse results. Agomir-17-5p decreased BBB permeability and antagomir-17-5p increased BBB permeability. TARBP2 as a RNA-binding protein (RBP) bound to SNHG7 and resulted in longer half-life of SNHG7. The decreased expression of miR-17-5p had a negative post-transcriptional regulation to NFATC3, leading to the increased expression of NFATC3. In addition, SNHG7 regulated NFATC3 expression by acting as a molecule sponge targeting to miR-17-5p. NFATC3 inhibited TJ proteins expression by functioning as a transcription factor. TARBP2/SNHG7/miR-17-5p/NFATC3 pathway implied a potential mechanism in studies of BBB changes in AD pathological progression.

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MicroRNA-132-3p alleviates neuron apoptosis and impairments of learning and memory abilities in Alzheimer’s disease by downregulation of HNRNPU stabilized BACE1

Cited by 20 publications

References 37 publications

A novel lncRNA RP11-386G11.10 reprograms lipid metabolism to promote hepatocellular carcinoma progression

A novel lncRNA RP11-386G11.10 reprograms lipid metabolism to promote hepatocellular carcinoma progression

Mechanism of miR-132-3p Promoting Neuroinflammation and Dopaminergic Neurodegeneration in Parkinson’s Disease

TARBP2-stablized SNHG7 regulates blood-brain barrier permeability by acting as a competing endogenous RNA to miR-17-5p/NFATC3 in Aβ-microenvironment

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