Publications by authors named "Xiaoyang Yuan"

10 Publications

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1,25-Dihydroxyvitamin D3 Supplementation during Pregnancy Is Associated with Allergic Rhinitis in the Offspring by Modulating Immunity.

J Immunol Res 2021 14;2021:6638119. Epub 2021 Apr 14.

Department of Otolaryngology, Affiliated Hangzhou First People's Hospital, Zhejiang University School of Medicine, Hangzhou, Zhejiang 310006, China.

Background: Maternal supplementation with 1,25-dihydroxyvitamin D3 (VD3) has immunologic effects on the developing fetus through multiple pathways. This study was aimed at investigating the effects of VD3 supplementation on immune dysregulation in the offspring during allergic rhinitis.

Methods: Different doses of VD3 as well as control were given to pregnant female mice. Ovalbumin (OVA) challenge and aluminum hydroxide gel in sterile saline were used to induce allergic rhinitis in offspring mice. Nasal lavage fluids (NLF) were collected, and eosinophils were counted in NLF 24 hours after the OVA challenge. Th1, Th2, Th17, and Treg subtype-relevant cytokines, including IFN-, IL-4, IL-10, IL-17, TGF-, and OVA-IgE levels from the blood and NLF of offspring mice, were detected by the enzyme-linked immunosorbent assay (ELISA) method. The Treg subtype was analyzed by flow cytometry. Treg cells were purified from offspring and were adoptively transferred to OVA-sensitized allogenic offspring mice. The outcomes were assessed in allogenic offspring.

Results: Our data showed that VD3 supplementation significantly decreased the number of eosinophils, basophils, and lymphocytes in the peripheral blood and NLF. The proportion of CD4CD25FoxP3Tregs had a positive correlation with VD3 in a dose-dependent manner. The levels of serum IgE, IL-4, and IL-17 were decreased while the expressions of IFN-, IL-10, and TGF- were significantly enhanced in VD3 supplementation groups. Adoptive transfer CD4CD25FoxP3Tregs of VD3 supplementation groups promoted Th1 and suppressed Th2 responses in the offspring during allergic rhinitis.

Conclusion: Our findings indicated that low dose VD3 supply in pregnant mice's diet suppressed Th2 and Th17 responses in allergic rhinitis by elevating the Th1 subtype and the proportion of CD4CD25FoxP3Tregs in offspring. It suggested that low dose VD3 supply may have the potential to act as a new therapeutic strategy for allergic rhinitis.
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http://dx.doi.org/10.1155/2021/6638119DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8062205PMC
April 2021

Nrf2 exerts mixed inflammation and glucose metabolism regulatory effects on murine RAW264.7 macrophages.

Int Immunopharmacol 2019 Jun 23;71:198-204. Epub 2019 Mar 23.

Institute of Gerontology, Department of Geriatrics, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, 1095 JieFang Avenue, Wuhan, Hubei 430030, China. Electronic address:

Nuclear factor (erythroid-derived 2)-like 2 (Nrf2) is a transcription factor that mediates a broad range of cellular antioxidative, detoxification and anti-inflammatory effects. However, the precise mechanism by which Nrf2 regulates inflammation and metabolism in macrophages remains controversial and unclear. To further clarify the roles of Nrf2 in inflammation and glucose metabolism regulation, retrovirus-mediated knockdown of Nrf2 was performed in murine RAW264.7 macrophages, and the cells were stimulated with 100 ng/mL lipopolysaccharide for 24 h for M1 activation. qPCR and western blotting results indicated that Nrf2 knockdown significantly enhanced expression of the inflammatory genes Il1a and Il1b in unstimulated macrophages and increased expression of the inflammatory genes Il1a, Il1b, Il6, Il10, Ccl2, Ccl22, and CD38 but decreased that of Tnfa and Tgfb1 in M1 macrophages. Nrf2 knockdown also significantly elevated IL6 and IL10 secretion by M1 macrophages. Western blotting showed that Nrf2 knockdown reduced iNOS protein levels in resting macrophages and enhanced CD38 protein levels in both resting and M1 macrophages. The differential regulation of these macrophage inflammation and polarization markers by Nrf2 reveals multiple roles for Nrf2 in regulating inflammation in macrophages. Moreover, Nrf2 knockdown increased the Glu4 protein level and decreased AKT and GSK3β protein phosphorylation in M1 macrophages, suggesting multiple roles for Nrf2 in regulating glucose metabolism in macrophages. Overall, our results are the first to demonstrate mixed inflammation and glucose metabolism regulatory effects of Nrf2 in macrophages that may occur independent of its classic function in redox regulation. These findings support the potential of Nrf2 as a therapeutic target for the prevention and treatment of inflammation- and obesity-associated syndromes, including diabetes and atherosclerosis.
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http://dx.doi.org/10.1016/j.intimp.2019.03.023DOI Listing
June 2019

Sub-Nanomolar Methylmercury Exposure Promotes Premature Differentiation of Murine Embryonic Neural Precursor at the Expense of Their Proliferation.

Toxics 2018 Oct 10;6(4). Epub 2018 Oct 10.

Department of Biology, University of Ottawa, Ottawa, ON K1N 6N5, Canada.

Methylmercury (MeHg) is a ubiquitous environmental pollutant that is known to be neurotoxic, particularly during fetal development. However, the mechanisms responsible for MeHg-induced changes in adult neuronal function, when their exposure occurred primarily during fetal development, are not yet understood. We hypothesized that fetal MeHg exposure could affect neural precursor development leading to long-term neurotoxic effects. Primary cortical precursor cultures obtained from embryonic day 12 were exposed to 0 nM, 0.25 nM, 0.5 nM, 2.5 nM, and 5 nM MeHg for 48 or 72 h. Total Hg accumulated in the harvested cells in a dose-dependent manner. Not all of the concentrations tested in the study affected cell viability. Intriguingly, we observed that cortical precursor exposed to 0.25 nM MeHg showed increased neuronal differentiation, while its proliferation was inhibited. Reduced neuronal differentiation, however, was observed in the higher dose groups. Our results suggest that sub-nanomolar MeHg exposure may deplete the pool of neural precursors by increasing premature neuronal differentiation, which can lead to long-term neurological effects in adulthood as opposed to the higher MeHg doses that cause more immediate toxicity during infant development.
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http://dx.doi.org/10.3390/toxics6040061DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6315723PMC
October 2018

Magnetic suspension dynamic calibration device of measurement system for dynamic characteristics of sliding bearings.

Rev Sci Instrum 2017 Oct;88(10):104701

Key Laboratory of Education Ministry for Modern Design and Rotor-Bearing System, Xi'an Jiaotong University, Xi'an 710049, China.

A measurement system error is a key factor that disturbs the identification precision of sliding bearing's dynamic characteristic coefficients. The transfer process and influence rule of errors from a measurement system to dynamic characteristic coefficients are analyzed by solving the dynamic characteristic measurement model. In order to ensure that the identification errors are no more than 40%, the amplitude error and phase error of the transfer function of the measurement system should be controlled within 10% and 1°, respectively. A novel magnetic suspension calibration method of the measurement system, which generates a vibration through a noncontact electromagnetic force rather than a traditional contact force, is proposed. A magnetic dynamic calibration device is developed. The experiment results show that the device can make dynamic calibration at different frequencies successfully, which is favorable to improve the controllability of the calibration process and the stability of calibration results.
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http://dx.doi.org/10.1063/1.5004410DOI Listing
October 2017

Inactivation of MSH3 by promoter methylation correlates with primary tumor stage in nasopharyngeal carcinoma.

Int J Mol Med 2017 Sep 27;40(3):673-678. Epub 2017 Jun 27.

Department of Otolaryngology, Affiliated Hangzhou First People's Hospital of Nanjing Medical University, Hangzhou, Zhejiang 310006, P.R. China.

The aim of this study was to investigate the inactivation of the MutS homolog human 3 (MSH3) gene by promoter methylation in nasopharyngeal carcinoma (NPC). Methylation‑specific PCR, semi‑quantitative reverse transcription PCR and immunohistochemical analysis were used to detect methylation and the mRNA and protein expression levels of MSH3 in 54 cases of NPC tissues and 16 cases of normal nasopharyngeal epithelial (NNE) tissues. The association between promoter methylation and mRNA expression, and the mRNA and protein expression of the gene and clinical factors was analyzed. The promoter methylation of MSH3 was detected in 50% (27/54) of the primary tumors, but not in the 16 NNE tissues. The mRNA and protein expression levels were significantly decreased in the 54 cases of human NPC as compared to the 16 NNE tissues (P<0.05). The MSH3‑methylated cases exhibited significantly lower mRNA and protein expression levels than the unmethylated cases (P<0.05). The MSH3 mRNA and protein expression levels were significantly associated with the variable T stage (P<0.05); however, they did not correlate with the age and sex of the patients, or with the N stage, TNM classification or histopathological subtype (P>0.05). On the whole, MSH3 was frequently inactivated by promoter methylation and its mRNA and protein expression correlated with the primary tumor stage in NPC.
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http://dx.doi.org/10.3892/ijmm.2017.3044DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5547962PMC
September 2017

Nuclear factor E2-related factor 2 knockdown enhances glucose uptake and alters glucose metabolism in AML12 hepatocytes.

Exp Biol Med (Maywood) 2017 05 1;242(9):930-938. Epub 2017 Jan 1.

Institute on Aging, Department of Geriatrics, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei 430030, China.

Nuclear factor E2-related factor 2 (Nrf2) is a transcription factor known to induce the expression of a variety of antioxidant and detoxification genes. Recently, increasing evidence has revealed roles for Nrf2 in glucose, lipid, and energy metabolism; however, the exact functions of Nrf2 in hepatocyte biology are largely unclear. In the current study, the transient knockdown of Nrf2 via siRNA transfection enhanced the glucose uptake of fasting AML12 hepatocytes to 325.3 ± 11.1% ( P < 0.05) of that of untransfected control cells. The impacts of Nrf2 knockdown (NK) on the antioxidant system, inflammatory response, and glucose metabolism were then examined in AML12 cells under both high-glucose (33 mmol/L) and low-glucose (4.5 mmol/L) conditions. NK lowered the gene and protein expression of the anti-oxidases heme oxygenase-1 and NAD(P)H: quinone oxidoreductase 1 and increased p-eukaryotic initiation factor-2α, p-nuclear factor-κB p65, and its downstream proinflammatory factors, including interleukin-1 beta, tumor necrosis factor-α, matrix metalloproteinase 2, and matrix metalloproteinase 9, at the protein level. NK also altered the protein expression of fibroblast growth factor 21, glucose transporter type 4, insulin-like growth factor 1, forkhead box protein O1, p-AKT, and p-GSK3α/β, which are involved in glucose uptake, glycogenesis, and gluconeogenesis in AML12 cells. Our results provide a comprehensive understanding of the central role of Nrf2 in the regulation of glucose metabolism in AML12 hepatocytes, in addition to its classical roles in the regulation of redox signaling, endoplasmic reticulum stress and proinflammatory responses, and support the potential of Nrf2 as a therapeutic target for the prevention and treatment of obesity and other associated metabolic syndromes. Impact statement Increasing evidence supports the complexity of Nrf2 functions beyond the antioxidant and detoxification response. Previous in vivo studies employing either Nrf2-knockout or Nrf2-activated mice have achieved a similar endpoint: protection against an obese and insulin-resistant phenotype that includes impaired lipogenesis and gluconeogenesis in the liver. These apparently paradoxical observations led us to evaluate the impact of Nrf2 in liver cells in the absence of any influence from the systemic environment, including changes in the secretion of adipokines and proinflammatory cytokines by adipose tissues. In the present study, Nrf2 knockdown was sufficient to induce fundamental changes in the glucose metabolism of AML12 hepatocytes in addition to its classical cytoprotective functions. We also discuss similarities and differences between our in vitro study and previous in vivo studies, which may be helpful to dissect and better understand in vivo data that represents the culmination of both local and systemic alterations.
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http://dx.doi.org/10.1177/1535370217694435DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5407588PMC
May 2017

Inactivation of parkin by promoter methylation correlated with lymph node metastasis and genomic instability in nasopharyngeal carcinoma.

Tumour Biol 2017 Mar;39(3):1010428317695025

1 Department of Otolaryngology, Hangzhou First People's Hospital, Nanjing Medical University, Hangzhou, China.

This study aimed to investigate the inactivation of the parkin gene by promoter methylation and its relationship with genome instability in nasopharyngeal carcinoma. Parkin was considered as a tumor suppressor gene in various types of cancers. However, its role in nasopharyngeal carcinoma is unexplored. Genomic instabilities were detected in nasopharyngeal carcinoma tissues by the random amplified polymorphic DNA. The methylation-specific polymerase chain reaction, semi-quantitative reverse transcription polymerase chain reaction, and immunohistochemical analysis were used to detect methylation and mRNA and protein expression of parkin in 54 cases of nasopharyngeal carcinoma tissues and 16 cases of normal nasopharyngeal epithelia tissues, and in 5 nasopharyngeal carcinoma cell lines (CNE1, CNE2, TWO3, C666, and HONE1) and 1 normal nasopharyngeal epithelia cell line (NP69). mRNA expression of parkin in CNE1 and CNE2 was analyzed before and after methyltransferase inhibitor 5-aza-2-deoxycytidine treatment. The relationship between promoter methylation and mRNA expression, demethylation and mRNA expression, and mRNA and protein expression of the gene and clinical factors and genomic instabilities were analyzed. The mRNA and protein expression levels were significantly reduced in 54 cases of human nasopharyngeal carcinoma compared with 16 cases of normal nasopharyngeal epithelia. Parkin-methylated cases showed significantly lower mRNA and protein expression levels compared with unmethylated cases. After 5-aza-2-deoxycytidine treatment, parkin mRNA expression was restored in CNE1 and CNE2; 92.59% (50/54) of nasopharyngeal carcinoma demonstrated genomic instability. Parkin is frequently inactivated by promoter methylation, and its mRNA and protein expression correlate with lymph node metastasis and genomic instability. Parkin deficiency probably promotes tumorigenesis in nasopharyngeal carcinoma.
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http://dx.doi.org/10.1177/1010428317695025DOI Listing
March 2017

Methylation of the FOXP3 upstream enhancer as a clinical indicator of defective regulatory T cells in patients with acute coronary syndrome.

Am J Transl Res 2016 15;8(12):5298-5308. Epub 2016 Dec 15.

Department of Geriatrics, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology Wuhan 430030, China.

Atherosclerosis is an immune-mediated inflammatory process, which acts as the main cause of acute coronary syndrome (ACS). Regulatory CD4+CD25+FOXP3+T cells (Tregs) are thought to play a major role in inhibiting the formation and progression of atherosclerosis. However, the exact role played by Tregs in the pathogenesis of ACS is yet remained unclear. FOXP3 is a key regulator of Treg formation and function. Demethylation at the CpG-rich island of FOXP3 upstream enhancers can alter FOXP3 expression, and may affect Treg function during the development of ACS. This study investigated the immunosuppressive function and methylation status of a FOXP3 upstream enhancer in Tregs in ACS patients. Notably, Tregs from ACS patients exhibited a significantly lower immunosuppressive effect on Teffs. Furthermore, the methylation status of the FOXP3 upstream enhancer was significantly increased in ACS patients. Consistent with these observations, Tregs originated from ACS patients manifested significantly lower levels of FOXP3 mRNA. The immunosuppressive effect of Tregs on Teffs was compromised in ACS patients. Together, our data suggest that examination of the methylation status of the FOXP3 upstream enhancer might be a novel approach to diagnose ACS and to differentiate ACS subtypes.
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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5209483PMC
December 2016

Dynamic Calibration and Verification Device of Measurement System for Dynamic Characteristic Coefficients of Sliding Bearing.

Sensors (Basel) 2016 Jul 30;16(8). Epub 2016 Jul 30.

Key Laboratory of Education Ministry for Modern Design and Rotor-Bearing System, Xi'an Jiaotong University, Xi'an 41049, China.

The identification accuracy of dynamic characteristics coefficients is difficult to guarantee because of the errors of the measurement system itself. A novel dynamic calibration method of measurement system for dynamic characteristics coefficients is proposed in this paper to eliminate the errors of the measurement system itself. Compared with the calibration method of suspension quality, this novel calibration method is different because the verification device is a spring-mass system, which can simulate the dynamic characteristics of sliding bearing. The verification device is built, and the calibration experiment is implemented in a wide frequency range, in which the bearing stiffness is simulated by the disc springs. The experimental results show that the amplitude errors of this measurement system are small in the frequency range of 10 Hz-100 Hz, and the phase errors increase along with the increasing of frequency. It is preliminarily verified by the simulated experiment of dynamic characteristics coefficients identification in the frequency range of 10 Hz-30 Hz that the calibration data in this frequency range can support the dynamic characteristics test of sliding bearing in this frequency range well. The bearing experiments in greater frequency ranges need higher manufacturing and installation precision of calibration device. Besides, the processes of calibration experiments should be improved.
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http://dx.doi.org/10.3390/s16081202DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5017368PMC
July 2016

Enhanced penetration of exogenous EPCs into brains of APP/PS1 transgenic mice.

Am J Transl Res 2016 15;8(3):1460-70. Epub 2016 Mar 15.

Department of Geriatrics, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology Wuhan 430030, China.

The aim of this study was to investigate the repair function of exogenous Endothelial progenitor cells (EPCs) for brain microvascular damage of the APP/PS1 transgenic mouse model of Alzheimer's disease (AD). This study used a density-gradient centrifugation method to isolate mononuclear cells (MNCs) from mouse bone marrow, which were subsequently seeded and cultured. Cells were characterized by morphology and detection of the surface markers CD34 and CD133 at different time points by immunofluorescence (IF) and flow cytometry (FCM). Then, EPCs were transfected with GFP adenoviral vectors (GFP-EPCs). Wild-type (WT) and APP/PS1 transgenic mice both received GFP-EPCs injection through the tail vein, and using a PBS buffer injection as the control. Seven days later, the animals' brain tissue was isolated. Expression of GFP was detected by quantitative polymerase chain reaction (qPCR) and western-blot (WB), while the fluorescence of GFP within the brains of mice was observed under a fluorescence microscope. Higher mRNA and protein expression of GFP, accompanied with increased green fluorescence, were detected in the brain of GFP-EPCs-injected APP/PS1 mice, as compared with GFP-EPCs-injected WT mice. The results show that the APP/PS1 transgenic mouse model of AD exhibited enhanced penetration of exogenous EPCs into brains than the WT mice.
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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4859631PMC
May 2016