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Regulation and bioinformatic analysis of circ_0015891/miR-129-1-3p axis in methamphetamine-induced dopaminergic apoptosis

ABSTRACT: Regulation and bioinformatic analysis of circ_0015891/miR-129-1-3p axis in methamphetamine-induced dopaminergic apoptosis

PROVIDER: PRJNA875086 | ENA |

REPOSITORIES: ENA

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Regulation and bioinformatic analysis of circ_0015891/miR-129-1-3p axis in methamphetamine-induced dopaminergic apoptosis

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Project description:Primary cilium serves as a cellular “antenna” to sense environmental signals. Ciliogenesis requires the removal of CP110 to convert the mother centriole into the basal body. Actin dynamics is also critical for cilia formation. How these distinct processes are properly regulated remains unknown. Here we show that miR-129-3p, a microRNA conserved in the vertebrates, controlled cilia assembly by down-regulating both CP110 and four proteins critical for actin dynamics, Arp2, Toca1, abLIM1, and abLIM3. Consistently, blocking miR-129-3p repressed cilia formation in cultured mammalian cells, whereas its overexpression potently induced ciliogenesis in proliferating cells and extraordinary cilia elongation. Moreover, inhibition of miR-129-3p in zebrafish embryos suppressed cilia assembly in the Kupffer’s vesicle and pronephric duct, leading to developmental abnormalities including curved body, pericardial oedema, and randomised left-right patterning. Our results thus unravel a novel mechanism that orchestrates both the centriole-to-basal body transition and subsequent cilia assembly via microRNA-mediated posttranscriptional regulations. We want to find the targets of miR-129-3p by overexpressing miR-129-3p oligo or control oligo in hTERT-RPE1 cells. Through microarray analysis we could check the downregulated genes and these genes might be the targets of miR-129-3p.

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miR-129-3p control cilia assembly by regulating CP110 and actin dynamics [miR-129-3p overexpression]

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2019-12-08 | GSE121853 | GEO

Src modulates its oncogenic signaling via regulation of miRNA-129-3p [mRNA]

2019-12-08 | GSE121852 | GEO

Src modulates its oncogenic signaling via regulation of miRNA-129-3p

Project description:Src modulates its oncogenic signaling via regulation of miRNA-129-3p

| PRJNA498642 | ENA

Src modulates its oncogenic signaling via regulation of miRNA-129-3p [mRNA]

Project description:Src modulates its oncogenic signaling via regulation of miRNA-129-3p [mRNA]

| PRJNA498644 | ENA

Src modulates its oncogenic signaling via regulation of miRNA-129-3p [microRNA]

Project description:Src modulates its oncogenic signaling via regulation of miRNA-129-3p [microRNA]

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AVE0991 regulates HOTAIRM1/miR-223-3p/α-synuclein to improve behaviour and protect dopaminergic neurons in human α-syn (A53T) overexpressing mice

Project description:Objective: Parkinson's disease (PD) is part of a common type of neurodegenerative disease. AVE0991, a non-peptide analogue of Ang-(1-7), by which the progression of PD has been discovered to be ameliorated, but the specific mechanism whereby AVE0991 modulates the progression of PD remains unclear. Materials and Methods: During the study, the mice overexpressing of human α-syn(A53T) were established to simulate PD pathology, and we also constructed an in vitro model of mouse dopaminergic neurons overexpressing hα-syn(A53T). The [18F] FDG-PET/CT method was also employed to assess FDG uptake in human α-syn(A53T) overexpressing mice. Level of Lnc HOTAIRM1, miR-223-3p were detected via RT-qPCR. Flow cytometry was deployed to assay cell apoptosis. Results: AVE0991 improved behavior disorder and decreased α-syn expression in the substantia nigra in mice with Parkinson's disease. AVE0991 inhibited apoptosis of dopaminergic neurons overexpressing hα-syn(A53T) by LncRNA HOTAIRM1. MiR-223-3p binds to HOTAIRM1 as a ceRNA and directly targets α-syn. Conclusion: The angiotensin-(1–7) analogue AVE0991 targeted the HOTAIRM1/miR-223-3p axis to degrade α-synuclein in PD mice, and showed neuroprotection in vitro.

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