Role of microRNAs on adipogenesis, chronic low-grade inflammation, and insulin resistance in obesity

Cruz, Kyria Jayanne Clímaco; Oliveira, Ana Raquel Soares de; Morais, Jennifer Beatriz Silva; Silva, Juliana

doi:10.1016/j.nut.2016.10.003

Cited by 50 publications

(34 citation statements)

References 78 publications

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“…MicroRNAs (miRNAs) are diminutive noncoding RNAs with approximately 22 nucleotides . Plenty of evidence corroborates the fact that miRNAs are clinical biomarkers in assorted inflammatory diseases .…”

Section: Introductionmentioning

confidence: 97%

Retracted: Notoginsenoside R1 protects WI‐38 cells against lipopolysaccharide‐triggered injury via adjusting the miR‐181a/TLR4 axis

Qian

Shao

et al. 2019

J of Cellular Biochemistry

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Notoginsenoside R1 (NGR1) is a neoteric phytoestrogen extracted from Panax notoginseng, and possesses comprehensive pharmacological functions in multitudinous ailments. But, whether NGR1 is utilized in neonatal pneumonia is not clear. This research study aspired to disclose the protective activity of NGR1 in neonatal pneumonia. WI-38 cells were co-stimulated with NGR1 and lipopolysaccharide (LPS, 10 ng/mL), CCK-8 and flow cytometry assays were implemented for cell viability and apoptosis assessment. Real-time quantitative plymerase chain reaction (RT-qPCR), enzyme-linked immunosorbent assay (ELISA), and Western blot analysis were executed for inflammatory cytokine determination. MicroRNA-181a (miR-181a) expression was evaluated through RT-qPCR, simultaneously, the impact of miR-181a was estimated in NGR1 and LPS co-managed cells. Dual luciferase report assay was performed to disclose the relation between miR-181a and Toll-like receptor 4 (TLR4). The nuclear factor-κB (NF-κB) and TAK1/JNK pathways were ultimately appraised.We found that NGR1 decreased cell viability, evoked apoptosis and impeded interleukin-1β (IL-1β), IL-6, and tumor necrosis factor-α (TNF-α) expression and secretions in LPS-managed WI-38 cells. MiR-181a expression was enhanced by NGR1, and miR-181a inhibition inverted the impacts of NGR1 in LPSmanaged WI-38 cells. Besides, TLR4 was predicted to be a firsthand direct target of miR-181a. Furthermore, NGR1 hindered NF-κB and TAK1/JNK pathways through modulating TLR4. These discoveries disclosed the fact that NGR1 protected WI-38 cells against LPS-triggered injury via adjusting the miR-181a/ TLR4 and NF-κB and TAK1/JNK pathways. K E Y W O R D SmicroRNA-181a, neonatal pneumonia, NF-κB, notoginsenoside R1, TAK1/JNK, toll-like receptor 4 | INTRODUCTIONNeonatal pneumonia is a universal ailment among newborns, and is also a major reason for neonatal death. 1 Statistical evidence displays that about 156 million new events of neonatal pneumonia take place around the world each year, and 95% of neonatal pneumonia episodes happen in the developing countries. 2 The clinical manifestations of neonatal pneumonia comprise fever, cough, dyspnea, heart failure, sepsis, and even death. 3,4 The causes of neonatal pneumonia are multitudinous and are linked to malnutrition, unsafe sanitation,

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Section: Introductionmentioning

confidence: 97%

Retracted: Notoginsenoside R1 protects WI‐38 cells against lipopolysaccharide‐triggered injury via adjusting the miR‐181a/TLR4 axis

Qian

Shao

et al. 2019

J of Cellular Biochemistry

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“…Surprisingly, role of other biomolecules such as miRNAs has not been considered in plant-specific medicinal properties or augmented therapy. Although role of human's own miRNAs in various diseases have been reported earlier [19,20]. Numerous updations of plant miRNAs from different families of plant kingdom in miRBase [21] have provided a firm ground to the proposition of speculating the role of plant miRNAs as a potential strategy in augmented therapy.…”

Section: Introductionmentioning

confidence: 99%

Dietary plant miRNAs as an augmented therapy: cross-kingdom gene regulation

et al. 2018

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Cross-kingdom gene regulation by microRNAs (miRNAs) initiated a hot debate on the effective role of orally acquired plant miRNAs on human gene expression. It resulted in the expansion of gene regulation theories and role of plant miRNAs in cross-kingdom regulation of gene expression. This opened up the discussion that 'Whether we really get what we eat?' and 'Whether the orally acquired miRNAs really have a biologically important consequences after entering our digestive and circulatory system?' The reports of orally acquired plant miRNAs inside human alimentary canal have been a topic of discussion in the scientific community. The cross-kingdom gene regulations have raised our hopes to explore the exciting world of plant miRNAs as therapeutic potential and dietary supplements. However, there are reports which have raised concerns over any such cross-kingdom regulation and argued that technical flaws in the experiments might have led to such hypothesis. This review will give the complete understanding of exogenous application and cross-kingdom regulation of plant miRNAs on human health. Here, we provide update and discuss the consequences of plant miRNA mediated cross-kingdom gene regulation and possibilities for this exciting regulatory mechanism as an augmented therapy against various diseases. ARTICLE HISTORY

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“…Our results also indicated that HMGA2 and SREBF1 are important molecules involved in modulating GLUT4 expression. miRNAs consist of a group of small non-coding RNAs, some of which play key roles in modulating the functions of human bodies (25,34,35). Numerous miRNAs have been demonstrated to be involved in endocrine and metabolic diseases (36,37), and several miRNAs (e.g., miR-93 and miR-145) have been reported to be involved in the pathogenesis of PCOS (27)(28)(29)(30)(31)(38)(39)(40)(41)(42).…”

Section: Discussionmentioning

confidence: 99%

“…Recent studies have proposed that miRNAs are important gene regulators involved in human diseases, including endocrine and metabolic diseases (23,24). Some miRNAs have been found to play critical roles in modulating glucose homeostasis, and the aberrant expression of those miRNAs can result in insulin resistance that is often involved in the development of metabolic diseases (25,26). Several miRNAs (i.e.…”

Section: Introductionmentioning

confidence: 99%

MicroRNA-33b-5p is overexpressed and inhibits GLUT4 by targeting HMGA2 in polycystic ovarian syndrome: An in vivo and in vitro study

Yang

Jiang

Xiao³

et al. 2018

Oncol Rep

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Polycystic ovary syndrome (PCOS) is a common endocrine and metabolic disease, but its pathogenesis remains largely unknown. The present study explored the role of microRNA‑33b‑5p (miR‑33b‑5p) in PCOS pathogenesis, with a particular focus on its role in regulating glucose transporter 4 (GLUT4). A rat model of PCOS was developed by injecting female SD rats with insulin and HCG. miR‑33b‑5p, GLUT4, sterol regulatory element‑binding protein 1 (SREBF1), and high mobility group A2 (HMGA2) expression in rat ovarian tissues was examined by qRT‑PCR and immunohistochemistry. The effect of a high dose of either glucose or insulin on miR‑33b‑5p, GLUT4, SREBF1 and HMGA2 expression was also examined in cultured adipocytes by qRT‑PCR and western blotting. Additionally, the luciferase reporter assay and chromatin immunoprecipitation (ChIP) were used to explore the role of miR‑33b‑5p in regulating HMGA2, SREBF‑1 and/or GLUT4. Elevated levels of miR‑33b‑5p expression were detected in the ovarian tissues of insulin resistant PCOS rats, and those levels were negatively correlated with those of GLUT4, HMGA2 and SREBF1 expression (P<0.05). Immunohistochemistry studies revealed that GLUT4, SREBF1, and HMGA2 expression levels in the ovarian tissues of insulin resistant PCOS rats were significantly lower than those in other groups of rats. In cultured adipocytes, excess extracellular glucose or insulin increased miR‑33b‑5p expression but reduced GLUT4, SREBF1 and HMGA2 expression, whereas the levels of GLUT4, SREBF1 and HMGA2 were elevated by inhibition of miR‑33b‑5. HMGA2 could directly bind to the 5'‑promoter region of GLUT4 and promote its expression, and could also promote SREBF1 expression. Moreover, SREBF1 could also directly bind to the 5'‑promoter region of GLUT4 and promote its expression. Our findings revealed that miR‑33b‑5p was overexpressed in the ovarian tissues of insulin resistant PCOS rats, and thus may play an important role in the development of insulin resistance in PCOS patients. miR‑33b‑5p can inhibit GLUT4 production by targeting HMGA2, and in addition, HMGA2 and SREBF1 are important molecules involved in modulating GLUT4 expression.

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Role of microRNAs on adipogenesis, chronic low-grade inflammation, and insulin resistance in obesity

Cited by 50 publications

References 78 publications

Retracted: Notoginsenoside R1 protects WI‐38 cells against lipopolysaccharide‐triggered injury via adjusting the miR‐181a/TLR4 axis

Retracted: Notoginsenoside R1 protects WI‐38 cells against lipopolysaccharide‐triggered injury via adjusting the miR‐181a/TLR4 axis

Dietary plant miRNAs as an augmented therapy: cross-kingdom gene regulation

MicroRNA-33b-5p is overexpressed and inhibits GLUT4 by targeting HMGA2 in polycystic ovarian syndrome: An in vivo and in vitro study

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