Expression of miR-199a-3p in human adipocytes is regulated by free fatty acids and adipokines

Gu, Nan; You, Lianghui; Shi, Chunmei; Yang, Lei; Pang, Lei; Cui, Xianwei; Ji, Chenbo; Zheng, Wen; Guo, Xirong

doi:10.3892/mmr.2016.5379

Cited by 35 publications

(26 citation statements)

References 58 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Nonaka and coworkers also found increased levels of miR-19a-3p, miR-29b-3p, and miR-30a-5p in plasma and miR-19a-3p, miR-21-5p, miR-29b-3p, miR-30a-5p, miR-199b-5p, and miR-208a-3p in heart samples from chronic Chagas patients, which was correlated with miR-21 upregulation in TGF-β-stimulated fibroblasts [121]. These miRNAs can regulate distinct genes and mechanisms, such as miR-193b targeting of TGF-β2 [122], apoptosis by miR-338 targeting of apoptosis-associated tyrosine kinase (AATK), and can also be induced by pro-inflammatory cytokines, such as those observed for TNF-α and IL-6 stimulation, that upregulate miR-199a in human adipocytes [123].…”

Section: Trypanosoma-host Interactionsmentioning

confidence: 82%

MicroRNAs: Biological Regulators in Pathogen–Host Interactions

Acuña

Flöeter-Winter

Muxel

2020

Cells

View full text Add to dashboard Cite

An inflammatory response is essential for combating invading pathogens. Several effector components, as well as immune cell populations, are involved in mounting an immune response, thereby destroying pathogenic organisms such as bacteria, fungi, viruses, and parasites. In the past decade, microRNAs (miRNAs), a group of noncoding small RNAs, have emerged as functionally significant regulatory molecules with the significant capability of fine-tuning biological processes. The important role of miRNAs in inflammation and immune responses is highlighted by studies in which the regulation of miRNAs in the host was shown to be related to infectious diseases and associated with the eradication or susceptibility of the infection. Here, we review the biological aspects of microRNAs, focusing on their roles as regulators of gene expression during pathogen–host interactions and their implications in the immune response against Leishmania, Trypanosoma, Toxoplasma, and Plasmodium infectious diseases.

show abstract

Section: Trypanosoma-host Interactionsmentioning

confidence: 82%

MicroRNAs: Biological Regulators in Pathogen–Host Interactions

Acuña

Flöeter-Winter

Muxel

2020

Cells

View full text Add to dashboard Cite

show abstract

“…Recent studies all pointed to an inflamed and hypoxic milieu in RA synovium, which played an important role in the phenotypic transformation of FLS [ 4 ]. Of note, miR-199a-3p expression displays responsiveness to hypoxia [ 18 ] and pro-inflammatory cytokines [ 19 ], which may partially account for its aberrant expression in RA-FLS. In addition, the aberrant circulating level of miR-199a-3p and RB1 mRNA in RA patient plasma, which conforms to the same trend detected in RA-FLS, demonstrated a potential clinical usefulness of circulating miR-199a-3p and RB1 for RA monitoring.…”

Section: Discussionmentioning

confidence: 99%

MiR-199a-3p inhibits proliferation and induces apoptosis in rheumatoid arthritis fibroblast-like synoviocytes via suppressing retinoblastoma 1

Wangyang

Wang

et al. 2018

Bioscience Reports

View full text Add to dashboard Cite

Background Fibroblast-like synoviocytes (FLSs) that line the intimal synovium play a crucial role in the pathogenesis of rheumatoid arthritis (RA). miR-199a-3p is a highly conserved miRNA that has been shown to regulate a variety of growth behaviors in diverse cell types. However, the role of miR-199a-3p in RA-FLS is still unknown. Methods Here, we presented the first experimental evidence showing that miR-199a-3p was a critical regulator of RA-FLS function. Results miR-199a-3p expression was significantly reduced in RA-FLS compared with normal FLS. Ectopic expression of miR-199a-3p significantly inhibited RA-FLS proliferation and induced apoptosis, which was demonstrated by an increase in caspase-3 activity and Bax/Bcl-2 ratio. Our bioinformatics analysis identified Retinoblastoma 1 (RB1) gene to be a direct target of miR-199a-3p. In RA-FLS, miR-199a-3p directly targetted the 3′-UTR of RB1 mRNA and suppressed endogenous RB1 expression, whereas miR-199a-3p-resistant variant of RB1 was not affected. Silencing RB1 decreased cell proliferation and promoted apoptosis in RA-FLS, an effect comparable with miR-199a-3p overexpression. Enforced expression of RB1 partially restored cell proliferation and attenuated apoptosis in miR-199a-3p-overexpressing RA-FLSs. Conclusion In summary, miR-199a-3p is down-regulated in RA-FLS, and miR-199a-3p inhibits proliferation and induces apoptosis in RA-FLS, partially via targetting RB1. The miR-199a-3p/RB1 pathway may represent a new therapeutic target for RA.

show abstract

“…miR-155, miR-199a and miR-101 directly target mTOR in different cell types [178][179][180][181][182]. Interestingly, all three of these miRNAs have been found at increased levels during obesity and other metabolic diseases, and have been proven to have a detrimental effect on vascular and endothelial function [65,[183][184][185][186][187][188]. The relationship between mTOR and endothelial dysfunction is well documented [189].…”

Section: Mirnas In the Regulation Of Autophagy Initiationmentioning

confidence: 99%

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

Expression of miR-199a-3p in human adipocytes is regulated by free fatty acids and adipokines

Cited by 35 publications

References 58 publications

MicroRNAs: Biological Regulators in Pathogen–Host Interactions

MicroRNAs: Biological Regulators in Pathogen–Host Interactions

MiR-199a-3p inhibits proliferation and induces apoptosis in rheumatoid arthritis fibroblast-like synoviocytes via suppressing retinoblastoma 1

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

Contact Info

Product

Resources

About