MicroRNA-21, induced by high glucose, modulates macrophage apoptosis via programmed cell death 4

Shang, Yuan-yuan; Fang, Ning-ning; Wang, Feng; Wang, Hui; Wang, Zhi-Hao; Tang, Mengxiong; Peng, Jie; Zhang, Yun; Zhang, Wei; Zhong, Ming

doi:10.3892/mmr.2015.3398

Cited by 22 publications

(17 citation statements)

References 40 publications

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“…In common, miRs bind to the 3′UTR of target genes and function through target gene-mediated modulation. 31 To further explore the miR-132-associated modulation, the possible target gene of miR-132 was screened by using miRanda software. TRAF6 has been reported to act as an adapter protein to control the inflammation.…”

Section: Discussionmentioning

confidence: 99%

Retracted: MicroRNA‐132 attenuates LPS‐induced inflammatory injury by targeting TRAF6 in neuronal cell line HT‐22

Wang

Liu

et al. 2018

J of Cellular Biochemistry

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Epilepsy is a common neurological disorder in the central nervous system. Inflammation disrupts the blood-brain barrier (BBB), which is responsible for maintaining brain homeostasis. This study was aimed to investigate the functional role of microRNA (miR)-132 in hippocampal HT-22 cells under lipopolysaccharide (LPS) stimulation. In vitro cell inflammatory model was constructed by LPS stimulation. Inflammatory cell injury was evaluated according to the alterations of cell viability, apoptosis, and expression of inflammatory cytokines. Then, miR-132 level after LPS treatment was assessed. Subsequently, miR-132 was abnormally expressed after cell transfection, and the effects of miR-132 on LPS-induced cell inflammatory injury as well as phosphorylated levels of key kinases in the NF-κB and MAPK kinase (MEK)/ERK pathways were determined. The target gene of miR-132 was virtually screened and verified, and whether miR-132 affected HT-22 cells under LPS stimulation through regulating the target gene was verified. The results showed that the level of miR-132 was down-regulated by LPS in HT-22 cells, and the LPS-induced inflammatory injury could be reduced by miR-132 overexpression. Then, the phosphorylated levels of kinases in the NF-κB and MEK/ERK pathways were decreased by miR-132 overexpression. Tumor necrosis factor receptor-associated factor 6 (TRAF6) was predicted and verified to be a target of miR-132. Moreover, the alterations induced by miR-132 overexpression in the LPS-treated HT-22 cells were abrogated by TRAF6 overexpression. Therefore, we drew the conclusion that LPS down-regulated miR-132 and miR-132 attenuated LPS-induced inflammatory cell injury by targeting TRAF6, along with the inhibition of the NF-κB and MEK/ERK pathways.

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Section: Discussionmentioning

confidence: 99%

Retracted: MicroRNA‐132 attenuates LPS‐induced inflammatory injury by targeting TRAF6 in neuronal cell line HT‐22

Wang

Liu

et al. 2018

J of Cellular Biochemistry

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“…46 MiR-21 exhibits increased expression in several forms of CVD 47 and is sensitive to high-concentration glucose treatment in macrophages, providing resistance to apoptosis induced by high glucose concentrations via programmed cell death 4 (PDCD4) regulation. 48 …”

Section: Discussionmentioning

confidence: 99%

Urinary chromium is associated with changes in leukocyte miRNA expression in obese subjects

et al. 2016

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Background/Objectives:Epidemiological studies suggest a link between chromium (Cr) status and cardiovascular disease. Increased urinary excretion of Cr was reported in subjects with diabetes compared with non-diabetic controls and those with non-diabetic insulin resistance. Epigenetic alterations have been linked to the presence of Cr, and microRNA (miRNA) expression has been implicated in the pathogenesis of metabolic diseases and cardiovascular diseases (CVDs). We investigated the association between Cr excretion and miRNA expression in leukocytes from obese subjects. We also examined the relationship between altered miRNA expression and selected clinical parameters to further investigate mechanisms linking Cr to metabolic diseases and CVDs.Subjects/Methods:We analyzed urinary Cr in 90 Italian subjects using inductively coupled plasma-mass spectrometry. Peripheral blood miRNA levels were screened with TaqMan Low-Density Array Human MicroRNA A. Cr level-associated expression of miRNAs was detected with multivariate regression analyses, and the top 10 candidate miRNAs were selected for validation. We also used multivariate regression analyses to assess possible associations between validated miRNAs and glycated hemoglobin (A1c) and blood pressure (BP). The validated miRNAs were further investigated by functional analysis with Ingenuity Pathway Analysis software.Results:Urinary Cr levels (mean: 0.35 μg/l; s.d.=0.24) ranged from 0.05 to 1.27 μg/l. In the screening phase, 43 miRNAs were negatively associated with Cr. Of the top 10 miRNAs selected for validation, nine (miR-451, miR-301, miR-15b, miR-21, miR-26a, miR-362-3p, miR-182, miR-183 and miR-486-3p) were downregulated in association with Cr (P-false discovery rate (FDR)<0.10). miR-451 expression was associated with A1c (β=–0.06; P=0.0416), whereas miR-486-3p expression was associated both with diastolic (β=2.1; P=0.004) and systolic BP (β=3.3; P=0.003).Conclusions:These results indicate that miR-451 and miR-486-3p are involved in the link between Cr levels and metabolic diseases and CVDs.

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“… 134 High glucose concentration upregulates microRNA-21 in macrophages. 135 MicroRNA-21 is a central regulator of cell proliferation and inflammation. 136 MicroRNA-21 promotes macrophage polarization toward proinflammatory M1 macrophages secreting IL-1β, and stimulates Th17 cell differentiation.…”

Section: Hyperglycemic Carbohydratesmentioning

confidence: 99%

Linking diet to acne metabolomics, inflammation, and comedogenesis: an update

Melnik¹

2015

CCID

189

177

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Acne vulgaris, an epidemic inflammatory skin disease of adolescence, is closely related to Western diet. Three major food classes that promote acne are: 1) hyperglycemic carbohydrates, 2) milk and dairy products, 3) saturated fats including trans-fats and deficient ω-3 polyunsaturated fatty acids (PUFAs). Diet-induced insulin/insulin-like growth factor (IGF-1)-signaling is superimposed on elevated IGF-1 levels during puberty, thereby unmasking the impact of aberrant nutrigenomics on sebaceous gland homeostasis. Western diet provides abundant branched-chain amino acids (BCAAs), glutamine, and palmitic acid. Insulin and IGF-1 suppress the activity of the metabolic transcription factor forkhead box O1 (FoxO1). Insulin, IGF-1, BCAAs, glutamine, and palmitate activate the nutrient-sensitive kinase mechanistic target of rapamycin complex 1 (mTORC1), the key regulator of anabolism and lipogenesis. FoxO1 is a negative coregulator of androgen receptor, peroxisome proliferator-activated receptor-γ (PPARγ), liver X receptor-α, and sterol response element binding protein-1c (SREBP-1c), crucial transcription factors of sebaceous lipogenesis. mTORC1 stimulates the expression of PPARγ and SREBP-1c, promoting sebum production. SREBP-1c upregulates stearoyl-CoA- and Δ6-desaturase, enhancing the proportion of monounsaturated fatty acids in sebum triglycerides. Diet-mediated aberrations in sebum quantity (hyperseborrhea) and composition (dysseborrhea) promote Propionibacterium acnes overgrowth and biofilm formation with overexpression of the virulence factor triglyceride lipase increasing follicular levels of free palmitate and oleate. Free palmitate functions as a “danger signal,” stimulating toll-like receptor-2-mediated inflammasome activation with interleukin-1β release, Th17 differentiation, and interleukin-17-mediated keratinocyte proliferation. Oleate stimulates P. acnes adhesion, keratinocyte proliferation, and comedogenesis via interleukin-1α release. Thus, diet-induced metabolomic alterations promote the visible sebofollicular inflammasomopathy acne vulgaris. Nutrition therapy of acne has to increase FoxO1 and to attenuate mTORC1/SREBP-1c signaling. Patients should balance total calorie uptake and restrict refined carbohydrates, milk, dairy protein supplements, saturated fats, and trans-fats. A paleolithic-like diet enriched in vegetables and fish is recommended. Plant-derived mTORC1 inhibitors and ω-3-PUFAs are promising dietary supplements supporting nutrition therapy of acne vulgaris.

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MicroRNA-21, induced by high glucose, modulates macrophage apoptosis via programmed cell death 4

Cited by 22 publications

References 40 publications

Retracted: MicroRNA‐132 attenuates LPS‐induced inflammatory injury by targeting TRAF6 in neuronal cell line HT‐22

Retracted: MicroRNA‐132 attenuates LPS‐induced inflammatory injury by targeting TRAF6 in neuronal cell line HT‐22

Urinary chromium is associated with changes in leukocyte miRNA expression in obese subjects

Linking diet to acne metabolomics, inflammation, and comedogenesis: an update

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