Involment of RAS/ERK1/2 signaling and MEF2C in miR-155-3p inhibition-triggered cardiomyocyte differentiation of embryonic stem cell

Ling, Xiang; Yao, Dongbo; Kang, Lumei; Zhou, Jing; Zhou, Ying; Dong, Hui-Fen; Zhang, Keping; Zhang, Lei; Chen, Hongping

doi:10.18632/oncotarget.21218

Cited by 15 publications

(16 citation statements)

References 48 publications

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“…Systemic administration has been proven to mitigate dysfunction and improve survival by targeting JNK . Nevertheless, miR-155 knockdown triggers apoptosis via induced liposaccharides [ 45 , 55 , 56 ]. In concert with miR-155, miR-146 downregulates expression of IRAK1 and TRAF6 , which are upstream activators of NF-κβ [ 5 ].…”

Section: Mirnas In Cardiomyocytesmentioning

confidence: 99%

“…IL-6 , along with NLRP3 , is mediated by miR-233 in monocytes [ 45 ]. Further, during myocarditis, miR-155 upregulates macrophages and CD4 + T lymphocytes [ 55 ]. Another strategic player during inflammation is miR-126, due to its control over endothelial VCAM-1 , which in turn help controls leukocyte trafficking and vasculature inflammation, potentially leading to cardiac repair by affecting the homing of hematopoietic progenitor cells [ 9 , 45 ].…”

Section: Mirnas In Cardiomyocytesmentioning

confidence: 99%

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A MicroRNA Perspective on Cardiovascular Development and Diseases: An Update

Islas

Moreno-Cuevas

2018

IJMS

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In this review, we summarize the latest research pertaining to MicroRNAs (miRs) related to cardiovascular diseases. In today’s molecular age, the key clinical aspects of diagnosing and treating these type of diseases are crucial, and miRs play an important role. Therefore, we have made a thorough analysis discussing the most important candidate protagonists of many pathways relating to such conditions as atherosclerosis, heart failure, myocardial infarction, and congenital heart disorders. We approach miRs initially from the fundamental molecular aspects and look at their role in developmental pathways, as well as regulatory mechanisms dysregulated under specific cardiovascular conditions. By doing so, we can better understand their functional roles. Next, we look at therapeutic aspects, including delivery and inhibition techniques. We conclude that a personal approach for treatment is paramount, and so understanding miRs is strategic for cardiovascular health.

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Section: Mirnas In Cardiomyocytesmentioning

confidence: 99%

Section: Mirnas In Cardiomyocytesmentioning

confidence: 99%

A MicroRNA Perspective on Cardiovascular Development and Diseases: An Update

Islas

Moreno-Cuevas

2018

IJMS

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“…MiRNAs play a wide range of roles in regulating life activities through posttranscriptional inhibition. MiRNAs are involved in multiple biological processes including cell proliferation, differentiation, and metabolism [13, 19, 29] by modulating specific genes. It has been shown that miRNAs are abnormally expressed in many types of diseases, including heart disease, inflammatory diseases, and especially cancers [20, 21, 30].…”

Section: Introductionmentioning

confidence: 99%

MiR-206-3p alleviates chronic constriction injury-induced neuropathic pain through targeting HDAC4

Wen

et al. 2019

Exp. Anim.

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It was identified that microRNAs were involved in the regulation of chronic neuropathic pain. However, the role of miR-206-3p in neuropathic pain was still unclear. In the current study, the role of miR-206-3p, a type of mature miR-206, in neuropathic pain was investigated. The potential mechanisms were also explored. We found that the expression of miR-206-3p decreased in the dorsal root ganglion (DRG) of chronic constriction sciatic nerve injury (CCI) rats, whereas the While histone deacetylase 4 (HDAC4) level increased. Further exploration showed that administration of a miR-206-3p mimic alleviated neuropathic pain and reduced the level of HDAC4, a predicted target of miR-206-3p. Overexpression of HDAC4 attenuated the effects of miR-206-3p on neuropathic pain. Our data revealed a miR-206-3p-HDAC4 signal that played a potentially important role in CCI-induced neuropathic pain.

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“…In murine systems, miR-155-3p has been shown to be upregulated in M1 (LPS and IFNγ) bone marrow-derived macrophages 15 , as well as in infiltrating T helper cells in experimental autoimmune encephalomyelitis 16 . As well as immune pathways, miR-155-3p has been reported to be regulated in other physiological process, including downregulation during cardiogenesis from embryonic stem cells 17 and in human glioblastoma cells during hypoxia 18 . It was also identified in a methylated form in mantle cell lymphoma (MCL; an aggressive B-cell non-Hodgkin's lymphoma), and demethylation resulted in increased expression, revealing tumour suppressing properties 19 .…”

Section: Introductionmentioning

confidence: 99%

Transient up-regulation of miR-155-3p by lipopolysaccharide in primary human monocyte-derived macrophages results in RISC incorporation but does not alter TNF expression

Simmonds¹

2019

Wellcome Open Res

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Background: The innate immune response is a tightly regulated process that reacts rapidly in response to pathogen-associated molecular patterns (PAMPs) such as lipopolysaccharide (LPS). Evidence is accumulating that microRNAs contribute to this, although few studies have examined the early events that constitute the “primary” response. Methods: LPS-dependent changes to miRNA expression were studied in primary human monocyte-derived macrophages (1°MDMs). An unbiased screen by microarray was validated by qPCR and a method for the absolute quantitation of miRNAs was also developed, utilising 5’ phosphorylated RNA oligonucleotide templates. RNA immunoprecipitation was performed to explore incorporation of miRNAs into the RNA-induced silencing complex (RISC). The effect of miRNA functional inhibition on TNF expression (mRNA and secretion) was investigated. Results: Of the 197 miRNAs expressed in 1°MDMs, only five were induced >1.5-fold. The most strongly induced was miR-155-3p, the partner strand to miR-155-5p, which are both derived from the MIR155HG/BIC gene (pri-miR-155). The abundance of miR-155-3p was induced transiently ~250-fold at 2-4hrs and then returned towards baseline, mirroring pri-miR-155. Other PAMPs, IL-1β, and TNF caused similar responses. IL-10, NF-κB, and JNK inhibition reduced these responses, unlike cytokine-suppressing mycolactone. Absolute quantitation revealed that miRNA abundance varies widely from donor-to-donor, and showed that miR-155-3p abundance is substantially less than miR-155-5p in unstimulated cells. However, at its peak there were 446-1,113 copies/cell, and miR-155-3p was incorporated into the RISC with an efficiency similar to miR-16-5p and miR-155-5p. Inhibition of neither miRNA affected TNF secretion after 2hrs in 1°MDMs, but technical challenges here are noted. Conclusions: Dynamic regulation of miRNAs during the primary response is rare, with the exception of miR-155-3p. Further work is required to establish whether its low abundance, even at the transient peak, is sufficient for biological activity and to determine whether there are specific mechanisms determining its biogenesis from miR-155 precursors

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Involment of RAS/ERK1/2 signaling and MEF2C in miR-155-3p inhibition-triggered cardiomyocyte differentiation of embryonic stem cell

Cited by 15 publications

References 48 publications

A MicroRNA Perspective on Cardiovascular Development and Diseases: An Update

A MicroRNA Perspective on Cardiovascular Development and Diseases: An Update

MiR-206-3p alleviates chronic constriction injury-induced neuropathic pain through targeting HDAC4

Transient up-regulation of miR-155-3p by lipopolysaccharide in primary human monocyte-derived macrophages results in RISC incorporation but does not alter TNF expression

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