Publications by authors named "Bao-Shi Yuan"

7 Publications

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The interaction of TAK1 and TAB1 enhances LPS-induced cytokine release via modulating NF-κB activation (Larimichthys crocea).

Fish Shellfish Immunol 2018 Mar 8;74:450-458. Epub 2018 Jan 8.

Fisheries College, Jimei University, Xiamen 361021, PR China. Electronic address:

Transforming growth factor-β-activating kinase 1 (TAK1) is triggered by foreign pathogenic infection and involves in proinflammatory response through the activation of nuclear factor-κB (NF-κB), which is specifically regulated by TAK1-binding protein 1 (TAB1). However, the expression and regulatory characterizations of TAK1 and TAB1 in fish immune response remain largely unknown. In the present study, the cDNA sequences of TAK1 (LcTAK1) and TAB1 (LcTAB1) were identified from large yellow croaker, Larimichthys crocea. The open reading frame (ORF) of LcTAK1 was 1725 bp in length, encoding 574 amino acids. The putative LcTAK1 protein contained a protein kinase domain and a C-terminal coiled-coil region. The ORF of LcTAB1 was 1518 bp encoding 505 amino acids. And a typical PP2Cc domain and a conserved sequence motif (PYVDFSQFYLLWGSDH) at C-terminal were identified in the predicted LcTAB1 protein. Multiple alignments showed that LcTAK1 shared 74.0-97.9% and LcTAB1 shared 37.4-95.8% sequence identities with TAK1 and TAB1 proteins from other species, respectively. Quantitative PCR analysis indicated that both LcTAK1 and LcTAB1 were broadly expressed in all examined tissues, with the most predominant expression in brain and the weakest expression in muscle, respectively. Subcellular localization revealed that both LcTAK1 and LcTAB1 expressed in the cytoplasm. In addition, LcTAK1 transcripts increased significantly in LCK cells after flagellin, LPS and poly I:C stimulation while LcTAB1 enhanced greatly after LPS and poly I:C challenge. Furthermore, the roles of them in NF-κB activation were investigated by overexpression of LcTAK1 and LcTAB1 in HEK293T cells. Our results revealed that NF-κB luciferase promoter expression could not be induced by overexpression of LcTAK1 or LcTAB1 alone, however, it could be induced by co-expression of LcTAK1 and LcTAB1 together. Moreover, the roles of LcTAK1 and LcTAB1 in immune response analysis showed that NF-κB activation enhanced significantly in co-overexpressed HEK293T cells following LPS and poly I:C stimulation. However, the expression levels of tumor necrosis factor (TNF)-α, Interleukin-6 (IL-6) and IL-8 were induced only after LPS challenge (p < .05). These findings suggested that the TAK1-TAB1 complex of large yellow croaker might play an important role in pro-inflammatory cytokines and chemokine release after LPS stimulation via inducing NF-κB activation.
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http://dx.doi.org/10.1016/j.fsi.2018.01.005DOI Listing
March 2018

Association between Helicobacter pylori infection and gallbladder diseases: A retrospective study.

J Gastroenterol Hepatol 2018 Jun 26;33(6):1207-1212. Epub 2018 Feb 26.

Department of Laboratorial Science and Technology, School of Public Health Peking University, Beijing, China.

Background And Aim: The association between Helicobacter pylori (H. pylori) and gallbladder diseases is still unclear and is controversial. We conducted a retrospective study to clarify the prevalence of gallbladder diseases and factors related to gallbladder diseases and relationships between H. pylori infection, gallstones, cholecystitis, and cholecystic polypus.

Methods: The retrospective study was performed at the Aerospace Center Hospital in Beijing. The subjects in this study were a healthy population who underwent health examinations at the hospital between 2012 and 2015. The logistic regression models were used to explore the relationships between H. pylori infection and gallbladder diseases.

Results: There were 7803 (43.4%) subjects with H. pylori infection, 995 (5.5%) with gallstones, 219 (1.2%) with cholecystitis, and 1003 (5.6%) with cholecystic polypus amongst 17 971 subjects, respectively. In subjects aged 45 years or less, the prevalence of gallstones in the H. pylori (+) group was lower than that in the H. pylori (-) group (odds ratio = 0.653; 95% confidence interval: 0.468-0.911; P = 0.012). The prevalence of cholecystic polypus in the H. pylori (+) group was significantly higher than that in the H. pylori (-) group (odds ratio = 1.160; 95% confidence interval: 1.012-1.328; P = 0.033).

Conclusions: Helicobacter pylori infection was related with cholecystic polypus and gallstones in a Chinese population.
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http://dx.doi.org/10.1111/jgh.14054DOI Listing
June 2018

Association of anaemia with Helicobacter pylori infection: a retrospective study.

Sci Rep 2017 10 18;7(1):13434. Epub 2017 Oct 18.

Department of Laboratorial Science and Technology, School of Public Health, Peking University, Beijing, 100191, P. R. China.

The role of Helicobacter pylori (H. pylori) infection in haematological system diseases is not well understood. We conducted this retrospective study to explore the association between H. pylori infection and anaemia in the Chinese population. This retrospective study was performed in Aerospace Center Hospital in Beijing. We derived the data from the registration system of the physical population between 2012-2016. Logistic regression models were used to explore the association between H. pylori infection and anaemia. Among 17,791 subjects, there were 7,804 (43.9%) subjects with H. pylori infection and 950 (5.3%) with anaemia. The prevalence of anaemia in the H. pylori (+) group was significantly higher than in the H. pylori (-) group after adjusting for age, sex, marriage, underlying diseases and body mass index. Compared to H. pylori (-), the OR of H. pylori (+) was 1.39 for moderate-to-severe anaemia and 1.05 for mild anaemia. The level of haemoglobin was lower in the H. pylori (+) group than in the H. pylori (-) group. This study indicates that H. pylori infection may be related to anaemia and haemoglobin level in the Chinese population.
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http://dx.doi.org/10.1038/s41598-017-13955-3DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5647388PMC
October 2017

Urate promotes SNCA/α-synuclein clearance via regulating mTOR-dependent macroautophagy.

Exp Neurol 2017 11 16;297:138-147. Epub 2017 Aug 16.

Department of Neurology and Suzhou Clinical Research Center of Neurological Disease, The Second Affiliated Hospital of Soochow University, Suzhou 215004, China; Institute of Neuroscience, Soochow University, Suzhou 215123, China; Jiangsu Key Laboratory of Translational Research and Therapy for Neuro-Psychiatric-Diseases, Soochow University, Suzhou, Jiangsu 215123, China. Electronic address:

Serum urate levels are reported to be significantly lowered in patients with Parkinson's disease (PD) and inversely correlated to the risk and progression of PD. However, the mechanism by which urate affects PD is poorly understood. Here we showed that treatment with uric acid (UA) resulted in an autophagy activity enhancement in PC12 cells in dose- and time-dependent manners, as indicated by LC3-II increase and P62 decrease. Moreover, UA was still able to increase the LC3-II level and the number of LC3 puncta in the presence of Bafilomycin A1, a lysosomal inhibitor. These changes of autophagic markers were preceded by mTOR inhibition and ULK1 activation. Co-treatment with 3-benzyl-5-((2-nitrophenoxy) methyl)-dihydrofuran-2(3H)-one (3BDO), an mTOR activator, abolished the UA-induced LC3-II increase. More importantly, UA reduced SNCA/α-synuclein accumulation in PC12 cells that overexpress wildtype or A53T mutant SNCA, and this was blocked by Bafilomycin A1 co-treatment. The in vivo study showed that UA administration was able to modulate the levels of autophagy markers, increase the autophagosome/autolysosome formation, and reduce SNCA accumulation in the midbrain of SNCA transgenic mice. Taken together, our findings suggest that UA could induce autophagy activation via an mTOR-dependent signaling and ameliorate SNCA accumulation. This implicates that urate-elevating agent may become a potential strategy for PD therapy.
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http://dx.doi.org/10.1016/j.expneurol.2017.08.007DOI Listing
November 2017

Impaired CBS-HS signaling axis contributes to MPTP-induced neurodegeneration in a mouse model of Parkinson's disease.

Brain Behav Immun 2018 Jan 1;67:77-90. Epub 2017 Aug 1.

Institute of Neuroscience, Soochow University, Suzhou 215123, China; Department of Neurology and Suzhou Clinical Research Center of Neurological Disease, The Second Affiliated Hospital of Soochow University, Suzhou 215004, China; Jiangsu Key Laboratory of Translational Research and Therapy for Neuro-Psychiatric-Diseases and College of Pharmaceutical Sciences, Soochow University, Suzhou, Jiangsu 215123, China. Electronic address:

Hydrogen sulfide (HS), a novel neuromodulator, is linked to the pathogenesis of several neurodegenerative disorders. Exogenous application of HS exerts neuroprotection via anti-inflammation and anti-oxidative stress in animal and cellular models of Parkinson's disease (PD). However, the role of endogenous HS and the contribution of its various synthases in PD remain unclear. In the present study, we found a decline of plasma and striatal sulfide level in 1-methy-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) induced PD mouse model. Interestingly, among the three HS generating enzymes, only cystathionine β-synthase (CBS) expression was largely reduced in the striatum of MPTP-treated mice. The in vitro study confirmed a significant decrease of CBS expression in 1-methyl-4-phenylpyridinium (MPP)-stimulated astrocytes and microglia, but not in neurons or SH-SY5Y dopaminergic cells. Striatal CBS overexpression, elicited by stereotaxic delivery with Cbs gene using recombinant adeno-associated-virus (rAAV-Cbs), successfully enhanced the sulfide level in the striatum and partially rescued the MPTP-induced dopaminergic neurotoxicity in the midbrain. Specifically, striatal CBS overexpression alleviated the motor deficits and dopaminergic neuron losses in the nigro-striatal pathway, with a concomitant inhibition of glial activation in MPTP-treated mice. Furthermore, compared to rAAV-Vector, rAAV-Cbs injection reduced the aberrant accumulation of nitric oxide and 3-nitrotyrosine (an indicator of protein nitration) in the striatum of MPTP-treated mice. Notably, it also attenuated the increase of nitrated α-synuclein level in MPTP mice. The in vitro study demonstrated that lentivirus-mediated CBS overexpression elevated the sulfide generation in glial cells. Moreover, glial CBS overexpression offered protection to midbrain dopaminergic neurons through repressing nitric oxide overproduction in both glial and neuronal cells induced by MPP. Taken together, our data suggest that impaired CBS-HS axis may contribute to the pathogenesis of PD, and that modulation of this axis may become a novel therapeutic approach for PD.
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http://dx.doi.org/10.1016/j.bbi.2017.07.159DOI Listing
January 2018

Association of obesity with infection: A retrospective study.

World J Gastroenterol 2017 Apr;23(15):2750-2756

Mei-Yan Xu, Jian Yin, Department of Nutrition, Aerospace Center Hospital, Beijing 100049, China.

Aim: To explore the association between () infection and obesity/weight gain in a Chinese population.

Methods: Our primary outcome was the change in body mass index (BMI). The generalized linear models were used to explore the association between infection and the change of BMI, and the logistic regression models were used to explore the association between infection and obesity.

Results: A total of 3039 subjects were recruited and analyzed, of which 12.8% were obese. The prevalence of infection was 53.9% (1639/3039) overall and 54.6% (212/388) in the obese subjects. The change of BMI in the (+) group was not significantly higher than that in the (-) group after adjustment for potential confounding factors [RR = 0.988, 95%CI: 0.924-1.057, = 0.729]. The prevalence of obesity decreased 1.1% in the (+) group and 0.5% in the (-) group. The RR of infection for obesity was 0.831 (95%CI: 0.577-1.197, = 0.321) after the adjustment.

Conclusion: infection was not associated with overweight/obesity observed from the retrospective study in this Chinese population.
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http://dx.doi.org/10.3748/wjg.v23.i15.2750DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5403754PMC
April 2017

Efficacy and safety of calcineurin inhibitor treatment for IgA nephropathy: a meta-analysis.

BMC Nephrol 2017 Feb 13;18(1):61. Epub 2017 Feb 13.

Department of Nephrology, Chinese PLA General Hospital, Chinese PLA Institute of Nephrology, State Key Laboratory of Kidney Diseases, National Clinical Research Center for Kidney Diseases, 28 Fuxing Road, Beijing, 100853, People's Republic of China.

Background: IgA nephropathy is the most common progressive glomerular disease to end stage renal failure worldwide. Calcineurin inhibitors (CNIs) is a selective immunosuppressant widely used in organ transplantation. The efficacy and safety of calcineurin inhibitors for the treatment of IgA nephropathy remain uncertain.

Methods: We performed a systematic literature search using the PubMed, Embase, Science Citation Index, Ovid evidence-based medicine, Chinese Biomedical Literature (CBM) and Chinese science and technology periodicals (CNKI, VIP, and Wan Fang) for randomized, controlled trials of CNIs therapy of IgA nephropathy. Complete remission rate (CR) was defined as proteinuria less than 0.5 or 0.3 g/d. Partial remission rate (PR) was defined as proteinuria reduced to at least half of the baseline measurement and an absolute value of >0.5 or 0.3 g/d.

Results: Seven relevant trials were conducted with 374 patients enrolled. CNIs plus medium/low-dose steroid had a higher CR (RR = 2.51 [95% CI,1.25 to 5.04], P = 0.02) compared to therapy with steroid alone or placebo, but were not significant on PR (RR = 0.87 [95% CI,0.32 to 2.38]; P = 0.78). Also, significant alterations were observed in proteinuria (weighted mean difference, -0.46 g/d,[95% CI:-0.55 to -0.24], P < 0.01) with no differences were found in serum creatinine (SCr) (weighted mean difference, 0.57,95% CI:-4.05 to 5.19; P = 0.78) and estimated glomerular filtration rate (eGFR) (weighted mean difference, 1.13,95% CI:-4.05 to 6.32; P = 0.34) level between the two groups. CNI therapy was associated with an increased risk for adverse events (RR = 2.21,95% CI:1.52 to 3.21, P < 0.01), such as gastrointestinal and neurological symptoms or hirsutism.

Conclusions: CNIs might provide renal protection in patients with IgAN, but at an increased risk of adverse events. Reliably defining the efficacy and safety of CNIs in IgAN requires a high-quality trial with a large sample size.
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http://dx.doi.org/10.1186/s12882-017-0467-zDOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5307812PMC
February 2017
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