Profiling peripheral micro<scp>RNA</scp>s in obesity and type 2 diabetes mellitus

Wu, Lang; Dai, Xiaojiang; Zhan, Junfang; Zhang, Yuxin; Zhang, Hongbin; Zhang, Hongbing; Zeng, Shenzheng; Xi, Wenbin

doi:10.1111/apm.12389

Cited by 50 publications

(36 citation statements)

References 23 publications

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“…Previous studies have shown that endogenous exosome production and content are affected by disease states in humans (31, 32) and can be used as biomarkers for diseases such as obesity and type 2 diabetes (33). However, it is unclear from these studies whether exosomes are playing a role in disease or if they are mere byproducts.…”

Section: Discussionmentioning

confidence: 99%

Rab27-Dependent Exosome Production Inhibits Chronic Inflammation and Enables Acute Responses to Inflammatory Stimuli

Alexander

Ramstead

Bauer

et al. 2017

The Journal of Immunology

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Extracellular vesicles, including exosomes, have recently been implicated as novel mediators of immune cell communication in mammals. However, roles for endogenously produced exosomes in regulating immune cell functions in vivo are just beginning to be identified. Here, we demonstrate that Rab27a and Rab27b double knockout (Rab27DKO) mice that are deficient in exosome secretion have a chronic, low-grade inflammatory phenotype characterized by elevated inflammatory cytokines and myeloproliferation. Upon further investigation, we found that some of these phenotypes could be complemented by WT hematopoietic cells or administration of exosomes produced by GM-CSF expanded bone marrow cells. Additionally, chronically inflamed Rab27DKO mice had a blunted response to bacterial LPS, resembling endotoxin tolerance. This defect was rescued by bone marrow exosomes from WT but not miR-155−/− cells suggesting that uptake of miR-155-containing exosomes is important for a proper LPS response. Further, we found that SHIP1 and IRAK-M, direct targets of miR-155 that are known negative regulators of the LPS response, were elevated in Rab27DKO mice and decreased following treatment with WT but not miR-155−/− exosomes. Together, our study finds that Rab27-dependent exosome production contributes to homeostasis within the hematopoietic system and appropriate responsiveness to inflammatory stimuli.

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Section: Discussionmentioning

confidence: 99%

Rab27-Dependent Exosome Production Inhibits Chronic Inflammation and Enables Acute Responses to Inflammatory Stimuli

Alexander

Ramstead

Bauer

et al. 2017

The Journal of Immunology

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“…Interestingly, some miRNAs have been identified as potential biomarkers for distinguishing obesity from T2DM [49, 50]. In an analysis of patient sera, Wu et al .…”

Section: Mirnas As Potential Biomarkers Of Metabolic Disordersmentioning

confidence: 99%

“…found the expression of the deregulated miRNAs, including miR-152, miR-17, miR-138, miR-593, miR-150, miR-205, miR-376a, miR-432-5p and miR-500a, to differ between a group of 25 healthy control subjects and groups of 25 patients with T2DM, 25 obese (OB) and 25 OB + T2DM patients. An analysis of the area under the curve (AUC) values based on receiver operating characteristic curves for each miRNA revealed that miR-152, miR-17, miR-593 and miR-138 alone can be used to distinguish patients with OB from those with T2DM, OB + T2DM or healthy subjects [49]. Similarly, Pescador et al .…”

Section: Mirnas As Potential Biomarkers Of Metabolic Disordersmentioning

confidence: 99%

MicroRNAs and metabolic disorders – where are we heading?

Śliwińska

Kasińska

Drzewoski

2017

aoms

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MicroRNAs (miRNAs, miRs) are short, non-coding molecules engaged in normal functioning of eukaryotic cells, as negative regulators of gene expression. Since the first discovery of miRNA in the early 1990s, hundreds of different miRNAs and their targets have been identified. A growing number of studies have aimed to search for microRNAs which have a key role in the regulation of insulin signaling and metabolic homeostasis. Recent evidence indicates that dysregulation of miRNA expression is involved in the development of various diseases, including type 2 diabetes mellitus (T2DM), obesity and cardiovascular diseases. This review summarizes the biogenesis of miRNAs and their role in pancreatic β cell biology, insulin signaling and metabolism. We also discuss recent findings of miRNAs associated with metabolic disorders and vascular diabetic complications, their diagnosis and therapeutic value. The PubMed database and published reference lists were searched for articles published between 1990 and 2016 using the following keywords: miRNA, miRNA and pancreas; miRNA and insulin; miRNA and type 2 diabetes mellitus, miRNA and obesity, and miRNA and microvascular or macrovascular diabetic complication. This review indicates that miRNA functioning is significantly different in metabolic diseases than in the normal condition.

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“…Transforming growth factor β1 (TGF‐β1) is the most important fibrotic factor known to be involved in the regulation of glomerular interstitial sediment synthesis and decomposition, cell growth, and formation of extracellular matrix . Increased expression of TGF‐β1 and activation of its downstream signaling pathway may be associated with fibrosis caused by various factors such as inflammatory factors, angiotensin II, and ischemia.…”

Section: Introductionmentioning

confidence: 99%

MiR‐182 inhibits kidney fibrosis by regulating transforming growth factor β1/Smad3 pathway in autosomal dominant polycystic kidney disease

Sun

Wang

et al. 2020

IUBMB Life

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The aim of the present study was to investigate the molecular mechanism of miR‐182 in kidney fibrosis in polycystic kidney disease (PKD). We measured the expression of miR‐182 in kidney tissue of autosomal dominant PKD. Additionally, we investigated the relationship between miR‐182 and fibrotic protein by transfecting miR‐182 mimics and miR‐182 inhibitor into polycystic kidney cyst‐lined epithelial cells, respectively. Furthermore, we observed the interaction between transforming growth factor β1 (TGF‐β1) and miR‐182 and fibrinogen factors of cyst‐lined epithelial cells after TGF‐β1 intervention, and measured the expression of Smad2 and Smad3 protein. Results are presented as follows: (a) MiR‐182 was positively correlated with fibrosis of cyst‐lined epithelial cells; (b) TGF‐β1 could induce fibrosis of cyst‐lined epithelial cells; (c) the expression of miR‐182 had a remarkably impact on the fibrosis induced by TGF‐β1, but had little effect on the expression of TGF‐β1; (d) the expression of Smad3 protein in TGF‐β1 induce‐cyst‐lined epithelial cells was increased. TGF‐β1 and miR‐182 promoting the fibrosis of polycystic kidney cyst‐lined epithelial cells may be mediated by the TGF‐β1/Smad3 signaling pathway, of which Smad3 was an important regulator.

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Profiling peripheral microRNAs in obesity and type 2 diabetes mellitus

Cited by 50 publications

References 23 publications

Rab27-Dependent Exosome Production Inhibits Chronic Inflammation and Enables Acute Responses to Inflammatory Stimuli

Rab27-Dependent Exosome Production Inhibits Chronic Inflammation and Enables Acute Responses to Inflammatory Stimuli

MicroRNAs and metabolic disorders – where are we heading?

MiR‐182 inhibits kidney fibrosis by regulating transforming growth factor β1/Smad3 pathway in autosomal dominant polycystic kidney disease

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