miR-374 promotes myocardial hypertrophy by negatively regulating vascular endothelial growth factor receptor-1 signaling

Lee, Jong Sub; Song, Dong Woo; Park, Jei Hyoung; Kim, Jin Ock; Cho, Chunghee; Kim, Do Han

doi:10.5483/bmbrep.2017.50.4.165

Cited by 15 publications

(14 citation statements)

References 24 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In contrast, the VEGF/VEGFR2 signaling pathway accelerates cardiac hypertrophy. Lee et al found that miR‐374 inhibited the VEGFR1 signalling pathway and activated GPCR signalling pathway by targeting the 3′‐UTR of VEGFR1 and cGMP‐dependent protein kinase‐1 to mediated pro‐hypertrophic processes.…”

Section: The Role Of Mir‐374 In Cardiovascular Diseasementioning

confidence: 99%

The latest progress on miR‐374 and its functional implications in physiological and pathological processes

Bian

Zhou

et al. 2019

J Cellular Molecular Medi

View full text Add to dashboard Cite

Non‐coding RNAs (ncRNAs) have been emerging players in cell development, differentiation, proliferation and apoptosis. Based on their differences in length and structure, they are subdivided into several categories including long non‐coding RNAs (lncRNAs >200nt), stable non‐coding RNAs (60‐300nt), microRNAs (miRs or miRNAs, 18‐24nt), circular RNAs, piwi‐interacting RNAs (26‐31nt) and small interfering RNAs (about 21nt). Therein, miRNAs not only directly regulate gene expression through pairing of nucleotide bases between the miRNA sequence and a specific mRNA that leads to the translational repression or degradation of the target mRNA, but also indirectly affect the function of downstream genes through interactions with lncRNAs and circRNAs. The latest studies have highlighted their importance in physiological and pathological processes. MiR‐374 family member are located at the X‐chromosome inactivation center. In recent years, numerous researches have uncovered that miR‐374 family members play an indispensable regulatory role, such as in reproductive disorders, cell growth and differentiation, calcium handling in the kidney, various cancers and epilepsy. In this review, we mainly focus on the role of miR‐374 family members in multiple physiological and pathological processes. More specifically, we also summarize their promising potential as novel prognostic biomarkers and therapeutic targets from bench to bedside.

show abstract

Section: The Role Of Mir‐374 In Cardiovascular Diseasementioning

confidence: 99%

The latest progress on miR‐374 and its functional implications in physiological and pathological processes

Bian

Zhou

et al. 2019

J Cellular Molecular Medi

View full text Add to dashboard Cite

show abstract

“…miR-26 plasma concentration was shown to be associated with AMI [43]. miR-374 was shown to be pro-hypertrophic and to be involved in VEGF-receptor-1 signaling [44]. The miR-26 family plays an essential role in angiogenesis, epithelial cell growth and tissue repair [45].…”

Section: Discussionmentioning

confidence: 99%

Anti-CD3 Antibody Treatment Reduces Scar Formation in a Rat Model of Myocardial Infarction

Wernly

Paar

Aigner

et al. 2020

Cells

View full text Add to dashboard Cite

Introduction: Antibody treatment with anti-thymocyte globulin (ATG) has been shown to be cardioprotective. We aimed to evaluate which single anti-T-cell epitope antibody alters chemokine expression at a level similar to ATG and identified CD3, which is a T-cell co-receptor mediating T-cell activation. Based on these results, the effects of anti-CD3 antibody treatment on angiogenesis and cardioprotection were tested in vitro and in vivo. Methods: Concentrations of IL-8 and MCP-1 in supernatants of human peripheral blood mononuclear cell (PBMC) cultures following distinct antibody treatments were evaluated by Enzyme-linked Immunosorbent Assay (ELISA). In vivo, anti-CD3 antibodies or vehicle were injected intravenously in rats subjected to acute myocardial infarction (AMI). Chemotaxis and angiogenesis were evaluated using tube and migration assays. Intracellular pathways were assessed using Western blot. Extracellular vesicles (EVs) were quantitatively evaluated using fluorescence-activated cell scanning, exoELISA, and nanoparticle tracking analysis. Also, microRNA profiles were determined by next-generation sequencing. Results: Only PBMC stimulation with anti-CD3 antibody led to IL-8 and MCP-1 changes in secretion, similar to ATG. In a rat model of AMI, systemic treatment with an anti-CD3 antibody markedly reduced infarct scar size (27.8% (Inter-quartile range; IQR 16.2-34.9) vs. 12.6% (IQR 8.3-27.2); p < 0.01). The secretomes of anti-CD3 treated PBMC neither induced cardioprotective pathways in cardiomyocytes nor pro-angiogenic mechanisms in human umbilical vein endothelial cell (HUVECs) in vitro. While EVs quantities remained unchanged, PBMC incubation with an anti-CD3 antibody led to alterations in EVs miRNA expression. Conclusion: Treatment with an anti-CD3 antibody led to decreased scar Cells 2020, 9, 295 2 of 19 size in a rat model of AMI. Whereas cardioprotective and pro-angiogenetic pathways were unaltered by anti-CD3 treatment, qualitative changes in the EVs miRNA expression could be observed, which might be causal for the observed cardioprotective phenotype. We provide evidence that EVs are a potential cardioprotective treatment target. Our findings will also provide the basis for a more detailed analysis of putatively relevant miRNA candidates.

show abstract

“…In a similar manner, miR-374a has been suggested to regulate ATG5 [227]. MiR-374a has been linked to metabolic disorder during obesity [228] and can promote heart dysfunction by negatively regulating vascular endothelial growth factor (VEGF) receptor-1 signaling [229].…”

Section: Mirnas In the Regulation Of Autophagy Elongationmentioning

confidence: 96%

MicroRNAs and obesity-induced endothelial dysfunction: key paradigms in molecular therapy

Ait‐Aissa¹,

Nguyen²,

Gabani³

et al. 2020

Cardiovasc Diabetol

View full text Add to dashboard Cite

The endothelium plays a pivotal role in maintaining vascular health. Obesity is a global epidemic that has seen dramatic increases in both adult and pediatric populations. Obesity perturbs the integrity of normal endothelium, leading to endothelial dysfunction which predisposes the patient to cardiovascular diseases. MicroRNAs (miRNAs) are short, single-stranded, non-coding RNA molecules that play important roles in a variety of cellular processes such as differentiation, proliferation, apoptosis, and stress response; their alteration contributes to the development of many pathologies including obesity. Mediators of obesity-induced endothelial dysfunction include altered endothelial nitric oxide synthase (eNOS), Sirtuin 1 (SIRT1), oxidative stress, autophagy machinery and endoplasmic reticulum (ER) stress. All of these factors have been shown to be either directly or indirectly caused by gene regulatory mechanisms of miRNAs. In this review, we aim to provide a comprehensive description of the therapeutic potential of miRNAs to treat obesity-induced endothelial dysfunction. This may lead to the identification of new targets for interventions that may prevent or delay the development of obesity-related cardiovascular disease.

show abstract

miR-374 promotes myocardial hypertrophy by negatively regulating vascular endothelial growth factor receptor-1 signaling

Cited by 15 publications

References 24 publications

The latest progress on miR‐374 and its functional implications in physiological and pathological processes

The latest progress on miR‐374 and its functional implications in physiological and pathological processes

Anti-CD3 Antibody Treatment Reduces Scar Formation in a Rat Model of Myocardial Infarction

MicroRNAs and obesity-induced endothelial dysfunction: key paradigms in molecular therapy

Contact Info

Product

Resources

About