MicroRNA-125a-3p is involved in early behavioral disorders in stroke-afflicted rats through the regulation of Cadm2

Liu, Yuqing; Li, Yunjun; Ren, Zhenxing; Si, Wenwen; Li, Yiwei; Wei, Gang; Zhao, Wenjing; Yuan, Tian; Chen, Dong Feng

doi:10.3892/ijmm.2017.3179

Cited by 7 publications

(7 citation statements)

References 46 publications

(43 reference statements)

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“…Furthermore, this effect was maintained when Cadm2 -knockout mice were crossed with the traditional obesity model, the Leptin -knockout mouse 11 . Rat models also demonstrate that increased Cadm2 (via a knockdown of a cadm2 regulator) reduced neurite outgrowth in response to ischemic damage 51 whilst errors in axon pathfinding and neurite outgrowth were observed in C adm2 -deficient chick embryos 52 . In vivo and in vitro studies of tumour models have demonstrated that increased expression of CADM2 mRNA or protein is associated with reduced cell viability, proliferation, migration and invasion in glioma 53 , retinoblastoma 54 , renal cell 55 , hepatocellular 56,57 , endometrial 58 , prostate 59 and oesophageal squamous cell carcinomas 60 .…”

Section: Discussionmentioning

confidence: 99%

Genetic variation in CADM2 as a link between psychological traits and obesity

Morris

Bailey

Baldassarre

et al. 2019

Sci Rep

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CADM2 has been associated with a range of behavioural and metabolic traits, including physical activity, risk-taking, educational attainment, alcohol and cannabis use and obesity. Here, we set out to determine whether CADM2 contributes to mechanisms shared between mental and physical health disorders. We assessed genetic variants in the CADM2 locus for association with phenotypes in the UK Biobank, IMPROVE, PROCARDIS and SCARFSHEEP studies, before performing meta-analyses. A wide range of metabolic phenotypes were meta-analysed. Psychological phenotypes analysed in UK Biobank only were major depressive disorder, generalised anxiety disorder, bipolar disorder, neuroticism, mood instability and risk-taking behaviour. In UK Biobank, four, 88 and 172 genetic variants were significantly (p < 1 × 10 −5 ) associated with neuroticism, mood instability and risk-taking respectively. In meta-analyses of 4 cohorts, we identified 362, 63 and 11 genetic variants significantly (p < 1 × 10 −5 ) associated with BMI, SBP and CRP respectively. Genetic effects on BMI, CRP and risk-taking were all positively correlated, and were consistently inversely correlated with genetic effects on SBP, mood instability and neuroticism. Conditional analyses suggested an overlap in the signals for physical and psychological traits. Many significant variants had genotype-specific effects on CADM2 expression levels in adult brain and adipose tissues. CADM2 variants influence a wide range of both psychological and metabolic traits, suggesting common biological mechanisms across phenotypes via regulation of CADM2 expression levels in adipose tissue. Functional studies of CADM2 are required to fully understand mechanisms connecting mental and physical health conditions.

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Section: Discussionmentioning

confidence: 99%

Genetic variation in CADM2 as a link between psychological traits and obesity

Morris

Bailey

Baldassarre

et al. 2019

Sci Rep

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“…In these studies, miR-125a-3p was shown to play a significant role in tumour cells; it can inhibit tumour growth and invasion and promote apoptosis [21][22][23] and can be a novel biomarker for early-stage colon cancer [24]. MiR-125a-3p is also reported to be involved in early behavioural disorders in stroke-afflicted rats through the regulation of Cadm2 [25] and in THP-1 macrophage differentiation and apoptosis [26]. In addition, miR-125a-3p plays roles in systemic lupus erythematous [27], morbid obesity [28] and orofacial inflammatory pain [29].…”

Section: Discussionmentioning

confidence: 99%

MicroRNA-125a-3p affects smooth muscle cell function in vascular stenosis

Chang

Zhang

et al. 2019

Journal of Molecular and Cellular Cardiology

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Many studies have indicated that microRNAs are closely related to the process of peripheral arterial disease (PAD). Previously, we found that microRNA-125a-3p (miR-125a-3p) in restenotic arteries after interventional therapy of lower extremity vessels was notably decreased compared with that of normal control arteries. However, its role in the development of vascular stenosis is not yet clearly understood. The purpose of this study was to investigate the expression, regulatory mechanism and function of miR-125a-3p in the process of vascular stenosis. Methods and results: Quantitative reverse-transcription polymerase chain reaction assays indicated that miR-125a-3p in restenotic arteries after interventional therapy was significantly lower than that in normal control arteries. Immunofluorescence and in situ hybridization co-staining assays in arterial sections demonstrated that miR-125a-3p was mainly expressed in the medial smooth muscle layer. Transfection of miR-125a-3p mimics into cultured vascular smooth muscle cells (VSMCs) effectively inhibited cell proliferation and migration. Then, western blot and luciferase activity assays showed that recombinant human mitogen-activated protein kinase 1 (MAPK1) was a functional target of miR-125a-3p and was involved in miR-125a-3p-mediated cell effects. Finally, the lentiviral infection of miR-125a-3p in balloon-injured rat carotid vascular walls showed that miR-125a-3p overexpression significantly reduced the probability of neointimal membrane production. Conclusions: miR-125a-3p can effectively inhibit the function of VSMCs and the occurrence of vascular stenosis by targeting MAPK1. This study introduces a new molecular mechanism of PAD. We show that regulation of the miR-125a-3p level has the potential to provide a new treatment for PAD and other proliferative vascular diseases. MicroRNAs are highly conserved single-stranded, non-coding RNA

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“…MiR-125a-5p has also been shown to be upregulated in macrophages following oxidized LDL exposure and inhibition of miRNA-125a-5p by a complimentary binding miRNA "antagomiR" increases lipid uptake by macrophages and enhances the expression of LOX-1 [3]. MiR-125a-3p is involved in behavioural disorders in animal models of MCAO by regulating cell adhesion molecule 2 (Cadm2) [13]. Bioinformatics analyses unanimously suggest that miR-125a-5p levels are elevated in acute ischemic stroke samples and healthy controls [23,27].…”

Section: Introductionmentioning

confidence: 99%

MiR-125a-5p silencing inhibits cerebral ischemia-induced injury through targeting IGFBP3

Song¹,

Xu²,

Zhong³

et al. 2021

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Dysregulated microRNAs (miRNAs) are crucial regulators of cerebrovascular conditions, including ischemic stroke. Circulating miR-125a-5p is associated with ischemic stroke and may have clinical utility as an early diagnostic biomarker. This study conducted a series of experiments that were designed to elucidate the regulatory action of miR-125a-5p in ischemic brain injury and its underlying mechanisms. The results of this study found that the expression of miR-125a-5p was increased in BV2 microglial cells under oxygen-glucose deprivation/reoxygenation (OGD/R) setting, as well as in rat brain tissue after middle cerebral artery occlusion (MCAO). OGD/R triggered BV2 microglial cell apoptosis, whereas downregulation of miRNA-125a-5p suppressed the apoptosis rate in OGD/R-induced BV2 microglial cells. Subsequently, insulin-like growth factor binding protein 3 (IGFBP3) is a molecular target of miR-125a-5p, and IGFBP3 knockdown reversed the effects of miR-125a-5p inhibitor on BV2 microglial cells in vitro. These data supported the fact that miR-125a-5p silencing protects against cerebral ischemia-induced injury by targeting IGFBP3.

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MicroRNA-125a-3p is involved in early behavioral disorders in stroke-afflicted rats through the regulation of Cadm2

Cited by 7 publications

References 46 publications

Genetic variation in CADM2 as a link between psychological traits and obesity

Genetic variation in CADM2 as a link between psychological traits and obesity

MicroRNA-125a-3p affects smooth muscle cell function in vascular stenosis

MiR-125a-5p silencing inhibits cerebral ischemia-induced injury through targeting IGFBP3

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