MiR-136 controls neurocytes apoptosis by regulating Tissue Inhibitor of Metalloproteinases-3 in spinal cord ischemic injury

Jin, Rilong; Xu, Sanzhong; Lin, Xiang; Shen, Miaoda

doi:10.1016/j.biopha.2017.07.053

Cited by 24 publications

(18 citation statements)

References 22 publications

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“…It is also significant to note that overexpressed miR-136-3p caused remarkable increase in proliferation and migration, accompanied by diminished apoptosis of HCY-stressed CMECs. These findings were largely consistent with a previously conducted study, where the treatment of miR-136 mimics protected neurocytes against injury that was induced by hypoxia in a spinal cord ischemic injury rat model [38].…”

Section: Discussionsupporting

confidence: 92%

Overexpression of microRNA-136-3p Alleviates Myocardial Injury in Coronary Artery Disease via the Rho A/ROCK Signaling Pathway

Lin

Dan

2020

Kidney Blood Press Res

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KeywordsCoronary artery disease · MicroRNA-136-3p · Cardiac microvascular endothelial cells · EIF5A2 · Rho A/ROCK signaling pathway Abstract Objective: Coronary artery disease (CAD) is a cardiovascular disease that poses a fatal threat to human health, and the identification of potential biomarkers may help to delineate its pathophysiological mechanisms. Accumulating evidence has implicated microRNAs (miRNAs) in the pathogenesis and development of cardiovascular diseases. The present study aims to identify the expression of miRNA-136-3p (miR-136-3p) in CAD and further investigate its functional relevance in myocardial injury both in vitro and in vivo. Methods: Initially, CAD models were induced in rats by high-fat diet and intraperitoneal injection of pituitrin. Next, the effect of overexpressed miR-136-3p on cardiac function and pathological damage in myocardial tissue, cardiomyocyte apoptosis, oxidative stress and inflammatory response were assessed in CAD rats. Rat cardiac microvascular endothelial cells (CMECs) were isolated and cultured by the tissue explant method, and the CMEC injury model was induced by homocysteine (HCY). The function of miR-136-3p in vitro was further evaluated. Results: miR-136-3p was poorly expressed in the myocardial tissue of CAD rats and CMEC injury models. In vivo assays indicated that overexpressed miR-136-3p could improve cardiac function and alleviate pathological damage in myocardial tissue, accompanied by reduced oxidative stress and inflammatory response. Moreover, in vitro assays suggested that overexpression of miR-136-3p enhanced proliferation and migration while inhibiting apoptosis of HCY-stressed CMECs. Notably, we revealed that EIF5A2 was a target gene of miR-136-3p, and miR-136-3p inhibited EIF5A2 expression and activation of the Rho A/ROCK signaling pathway. Conclusion: In conclusion, the overexpression of miR-136-3p could potentially impede myocardial injury in vitro and in vivo in CAD through the blockade of the Rho A/ROCK signaling pathway, highlighting a potential miR-136-3p functional relevance in the treatment of CAD.

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Section: Discussionsupporting

confidence: 92%

Overexpression of microRNA-136-3p Alleviates Myocardial Injury in Coronary Artery Disease via the Rho A/ROCK Signaling Pathway

Lin

Dan

2020

Kidney Blood Press Res

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“…Spinal cord injury (SCI) is characterized by high disability and mortality due to the complicated nature of this disease despite various treatment strategies have been developed (Branco et al, 2007;Silva et al, 2014;Ghali & Neuroscience 2017). Numerous evidences have suggested that the pathogenesis of SCI is associated with a variety of miRNAs including miR-137 (Gao et al, 2018), miR-221 (Zhao et al, 2018), miR-9 (Xu et al, 2016), and miR-136 (Jin et al, 2017). In our study, miR-139-5p was confirmed to be related to SCI with decreased expression in SCI rat model.…”

Section: Discussionsupporting

confidence: 69%

“…miR-9 down-regulated the expression of monocyte chemotactic proteininduced protein 1 (MCPIP1) and led to the suppression of neuronal cell apoptosis in acute spinal cord injury (Xu et al, 2016). miR-136 protected neurocytes against apoptosis by targeting tissue inhibitor of metalloproteinases-3 in spinal cord ischemia injury model (Jin et al, 2017).…”

Section: Introductionmentioning

confidence: 99%

MiR-139-5p alleviates neural cell apoptosis induced by spinal cord injury through targeting TRAF3

2020

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Spinal cord injury (SCI) is a neurological trauma that causes loss of locomotor function and sensory deficit. Previous studies showed that miRNAs play a crucial role in SCI. This study further evaluated the potential role of miR-139-5p in the neural cell apoptosis after SCI in rats. A rat SCI model was successfully established and miR-139-5p expression level in SCI rats was down-regulated compared to the sham group (sham operation group) determined by qRT-PCR. MiR-139-5p overexpression via administration with miR-139-5p agomir improved locomotor functional recovery, attenuated allodynia and hyperalgesia and alleviated neural cell apoptosis in SCI rats. In addition, TRAF3 (TNF receptor-associated factor 3 ) was identified to be a target of miR-139-5p by searching the proposed target genes in TargetScan 7.1 database. Co-transfection of miR-139-5p agomir and adenovirus of TRAF3 plasmids significantly improved functional recovery and alleviated neural cell apoptosis. Therefore, TRAF3 mediated the anti-apoptosis effect of miR-139-5p in SCI rats and miR-139-5p could be a promising candidate for SCI therapy by alleviating neural cell apoptosis through targeting TRAF3.

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“…In case of neurodegeneration, oxidative stress dependent neurotoxicity and apoptosis was linked with following microRNAs: miR-98 , miR-132 , miR-153 , miR-200a , miR-186 , miR-221 , miR-196a , miR-22 , miR-107 , miR-223 , miR-320 , miR-125b , miR-181 , miR-365 , miR-193 , miR-49 , miR-378 , miR-25 , miR-30d-5p , miR-26b , miR-592-5p , miR-153 , miR-155 , miR-212 , miR-183/96/182 cluster, miR-146a [94,151,153,154,155,156,157,158,159,160,161,162,163,164,165,166,167,168,169,170,171,172,173,174,175,176,177,178,179,180,181,182,183,184,185,186]. MicroRNAs that are linked to the therapy resistance and sensitivity are the ones engaged in cancer cell survival.…”

Section: More About Microrna In Neuropathologymentioning

confidence: 99%

MicroRNA in Brain pathology: Neurodegeneration the Other Side of the Brain Cancer

Godlewski

Lenart

Salińska

2019

ncRNA

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The mammalian brain is made up of billions of neurons and supporting cells (glial cells), intricately connected. Molecular perturbations often lead to neurodegeneration by progressive loss of structure and malfunction of neurons, including their death. On the other side, a combination of genetic and cellular factors in glial cells, and less frequently in neurons, drive oncogenic transformation. In both situations, microenvironmental niches influence the progression of diseases and therapeutic responses. Dynamic changes that occur in cellular transcriptomes during the progression of developmental lineages and pathogenesis are controlled through a variety of regulatory networks. These include epigenetic modifications, signaling pathways, and transcriptional and post-transcriptional mechanisms. One prominent component of the latter is small non-coding RNAs, including microRNAs, that control the vast majority of these networks including genes regulating neural stemness, differentiation, apoptosis, projection fates, migration and many others. These cellular processes are also profoundly dependent on the microenvironment, stemness niche, hypoxic microenvironment, and interactions with associated cells including endothelial and immune cells. Significantly, the brain of all other mammalian organs expresses the highest number of microRNAs, with an additional gain in expression in the early stage of neurodegeneration and loss in expression in oncogenesis. However, a mechanistic explanation of the concept of an apparent inverse correlation between the odds of cancer and neurodegenerative diseases is only weakly developed. In this review, we thus will discuss widespread de-regulation of microRNAome observed in these two major groups of brain pathologies. The deciphering of these intricacies is of importance, as therapeutic restoration of pre-pathological microRNA landscape in neurodegeneration must not lead to oncogenesis and vice versa. We thus focus on microRNAs engaged in cellular processes that are inversely regulated in these diseases. We also aim to define the difference in microRNA networks between pro-survival and pro-apoptotic signaling in the brain.

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MiR-136 controls neurocytes apoptosis by regulating Tissue Inhibitor of Metalloproteinases-3 in spinal cord ischemic injury

Cited by 24 publications

References 22 publications

Overexpression of microRNA-136-3p Alleviates Myocardial Injury in Coronary Artery Disease via the Rho A/ROCK Signaling Pathway

Overexpression of microRNA-136-3p Alleviates Myocardial Injury in Coronary Artery Disease via the Rho A/ROCK Signaling Pathway

MiR-139-5p alleviates neural cell apoptosis induced by spinal cord injury through targeting TRAF3

MicroRNA in Brain pathology: Neurodegeneration the Other Side of the Brain Cancer

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