Correlation between DNA methylation and Thymic Stromal Lymphopoietin expression in asthmatic airway epithelial cells

Yan‑Li Li,Xi‑Qian Xing,Yi Xiao,Yan‑Hong Liu,Yu‑Shan Zhou,Min Zhuang,Chao‑Qian Li 한국유전학회 2020 Genes & Genomics Vol.42 No.12

Background: The overexpression of TSLP and DNA methylation in asthma were both risk factors the relationship was not clear. Objective: This study aimed to investigate the relationship between methylation status of TSLP promoter and mRNA/protein expression in asthmatic airway epithelial cells. Methods: Human bronchial epithelial cells were cultured in vitro and divided into: Control group, treated with PBS, model group, sensitized with LPS (10 μg/mL) for 12 h (37 °C, 5% CO2). Other groups were cultured with the pCMV3 plasmid (M + NC/pCMV), pGPH1 plasmid (M + NC/pGPH), DNMT1/pCMV3 plasmid (M + DNMT1/pCMV), and DNMT1/pGPH1 plasmid (M + DNMT1/pGPH) for 48 h. The expression of DNA methyltransferase 1 and TSLP were measured using real-time PCR and western blotting. Results: Compared with the control group, TSLP mRNA (1.00 ± 0.00 vs. 2.82 ± 0.81 vs. 1, P < 0.001) and protein (1.07 ± 0.04 vs. 1.46 ± 0.11, P < 0.01) were significantly greater, and the methylation of promoter was lower (92.75 ± 1.26 vs. 58.57 ± 3.34, P < 0.05) in the model group. Compared with the model group, TSLP mRNA (2.82 ± 0.81 vs. 1.17 ± 0.10, P < 0.001) decreased, but TSLP promoter methylation increased (58.57 ± 3.34 vs. 92.58 ± 7.30, P < 0.05) in M + DNMT1/pCMV. TSLP mRNA and protein were higher (2.82 ± 0.81 vs. 5.32 ± 0.21, P < 0.001; 1.46 ± 0.11 vs. 1.94 ± 0.11, respectively, P < 0.01), TSLP promoter methylation was lower (58.57 ± 3.34 vs. 33.57 ± 4.29, P < 0.05) in M + DNMT1/pGPH. Conclusions: Overexpression of TSLP in asthmatic airway epithelial cells may be regulated by DNA demethylation.

Improved lithium storage performance of CeO2-decorated SrLi2Ti6O14 material as an anode for Li-ion battery

Ying Li,Hong-Yan Liu,Ling-Na Shi,Yan-Rong Zhu,Ting-Feng Yi 한국공업화학회 2021 Journal of Industrial and Engineering Chemistry Vol.101 No.-

In this work, the CeO2-decorated SrLi2Ti6O14 anode was successfully prepared through a solid-state process. The space-charge effect induced by the internal adsorption of ions on the CeO2 surface can easilyresult in a formation of an excellent conductive interfacial layer between CeO2 and SrLi2Ti6O14. The goodelectrical contact between CeO2 and SrLi2Ti6O14 offers more active sites for the electrolyte storage andredox reaction, and promotes the intercalation/deintercalation of lithium ions, and thus improves therate performance and cycle stability. Due to its unique structure and composition, the CeO2-decoratedSrLi2Ti6O14 composites exhibit high reversible capacities, good cycle performance and outstanding rateperformance. Especially, the CeO2 (5 wt%)-decorated SrLi2Ti6O14 anode shows the most excellent electrochemicalperformance, which delivers a large charge capacity of 121.3 mAh g 1 and a capacity retentionof 94.48% after 100 cycles at 0.5 A g 1. However, the corresponding charge capacity and capacity retentionof pristine SrLi2Ti6O14 are 100.5 mAh g 1 and 86.77%, respectively. The CeO2(5 wt%)-decoratedSrLi2Ti6O14 with enhanced rate capacity, cycle stability and structural stability is a potential electrodematerial candidate for Li-ion battery.

CdSe@ZnS/ZnS quantum dots loaded in polymeric micelles as a pH-triggerable targeting fluorescence imaging probe for detecting cerebral ischemic area

Yang, Hong Yu,Fu, Yan,Jang, Moon-Sun,Li, Yi,Yin, Wen Ping,Ahn, Tae Kyu,Lee, Jung Hee,Chae, Heeyeop,Lee, Doo Sung Elsevier 2017 Colloids and surfaces. B, Biointerfaces Vol.155 No.-

<P><B>Abstract</B></P> <P>High photoluminescence (PL) quantum yield (QY), photostability CdSe@ZnS/ZnS core/multishell quantum dots (CM-QDs) were first applied for bioimaging. The solubility, stability and biocompatible of the fluorescence imaging probes were constructed by self-assembly of CM-QDs and pH-responsive methoxy poly(ethylene glycol)-poly(β-amino ester/amidoamine)-dodecylamine (mPEG-PAEA-DDA) multiblock copolymers. The resulting CM-QDs-loaded mPEG-PAEA-DDA micelles (CM-QDs-PEG-PAEA-DDA) exhibited lower cell cytotoxicity and higher fluorescence intensity than the core/shell CdSe@ZnS QDs-encapsulated mPEG-PAEA-DDA micelles (CS-QDs-PEG-PAEA-DDA). Moreover, the in vivo fluorescence imaging ability confirmed that the CM-QDs-PEG-PAEA-DDA can be employed as a pH-triggerable targeting imaging probe for detection of a rat bearing cerebral ischemia disease. Therefore, we believed that the CM-QDs-PEG-PAEA-DDA may be the next generation of fluorescence imaging probes for targeted diagnosis acidic pathological areas, using pH as a stimulus.</P> <P><B>Highlights</B></P> <P> <UL> <LI> CdSe@ZnS/ZnS QDs are synthesized and first applied for bioimaging. </LI> <LI> mPEG-PAEA-DDA copolymer showed pH-responsive property and the hydrolysis stability. </LI> <LI> CM-QDs-PEG-PAEA-DDA exhibited lower toxicity and higher fluorescent intensity. </LI> <LI> CM-QDs-PEG-PAEA-DDA has ability to target image for acidic brain ischemic area. </LI> </UL> </P> <P><B>Graphical abstract</B></P> <P>[DISPLAY OMISSION]</P>

Cell surface vimentin-targeted monoclonal antibody 86C increases sensitivity to temozolomide in glioma stem cells

Noh, Hyangsoon,Zhao, Qingnan,Yan, Jun,Kong, Ling-Yuan,Gabrusiewicz, Konrad,Hong, Sungguan,Xia, Xueqing,Heimberger, Amy B.,Li, Shulin Elsevier 2018 Cancer letters Vol.433 No.-

<P><B>Abstract</B></P> <P>Glioblastoma multiforme (GBM) is the most prevalent and aggressive brain tumor. The current standard therapy, which includes radiation and chemotherapy, is frequently ineffective partially because of drug resistance and poor penetration of the blood-brain barrier. Reducing resistance and increasing sensitivity to chemotherapy may improve outcomes. Glioma stem cells (GSCs) are a source of relapse and chemoresistance in GBM; sensitization of GSCs to temozoliomide (TMZ), the primary chemotherapeutic agent used to treat GBM, is therefore integral for therapeutic efficacy. We previously discovered a unique tumor-specific target, cell surface vimentin (CSV), on patient-derived GSCs. In this study, we found that the anti-CSV monoclonal antibody 86C efficiently increased GSC sensitivity to TMZ. The combination TMZ+86C induced significantly greater antitumor effects than TMZ alone in eight of 12 GSC lines. TMZ+86C–sensitive GSCs had higher CSV expression overall and faster CSV resurfacing among CSV<SUP>−</SUP> GSCs compared with TMZ+86C–resistant GSCs. Finally, TMZ+86C increased apoptosis of tumor cells and prolonged survival compared with either drug alone in GBM mouse models. The combination of TMZ+86C represents a promising strategy to reverse GSC chemoresistance.</P> <P><B>Highlights</B></P> <P> <UL> <LI> Anti-CSV monoclonal antibody 86C sensitize GSCs to TMZ treatment. </LI> <LI> GSCs with higher CSV expression are more sensitive to TMZ+86C. </LI> <LI> GSCs with higher CSV resurfacing rate among CSV<SUP>−</SUP> cells are more sensitive to TMZ+86C. </LI> <LI> TMZ+86C increased apoptosis and prolonged survival in GBM models. </LI> <LI> Tumor-specific CSV antibody 86C can efficiently target human GSCs to increase their sensitivity to TMZ. </LI> </UL> </P>

LPL gene Pvu II polymorphism and hypertriglycer-idemia: a meta-analysis involving 1,640 subjects

( Yan-yan Li ),( Yan-hong Zhou ),( Ge Gong ),( Hong-yu Geng ),( Xin-xing Yang ),( Xiang-ming Wang ),( Chuan-wei Zhou ),( Jian Xu ),( Yun Qian ) 대한내과학회 2017 The Korean Journal of Internal Medicine Vol.32 No.6

Background/Aims: Although lipoprotein lipase (LPL) gene Pvu II polymorphism has been associated with an increased risk of hypertriglyceridemia (HT), there is no clear consensus within the scientific community. Methods: A meta-analysis of 1,640 subjects from six individual studies was conducted to better elucidate the potential relationship between the LPL gene Pvu II polymorphism and HT within the Chinese population. Pooled odds ratios (ORs) and their corresponding 95% confidence intervals (CIs) were evaluated by using fixed effect models. Results: Our analysis indicated a significant association between LPL gene Pvu II polymorphism and HT within the Chinese population under allelic (OR, 1.550; 95% CI, 1.320 to 1.830; p = 1.158 × 10^-7), recessive (OR, 0.540; 95% CI, 0.390 to 0.750; p = 0.0002), dominant (OR, 1.889; 95% CI, 1.501 to 2.377; p = 5.960 × 10^-8), homozygous (OR, 2.167; 95% CI, 1.531 to 3.067; p = 1.242 × 10^-5), heterozygous (OR, 1.810; 95% CI, 1.419 to 2.309; p = 1.842 × 10^-6), and additive genetic models (OR, 1.553; 95% CI, 1.320 to 1.828; p = 1.158 × 10^-7). Conclusions: Because LPL gene Pvu II restriction fragment length polymorphism polymorphism was associated with an elevated risk of HT, the P+ allele carriers of the LPL gene might be predisposed to HT.

Disruption of endothelial barrier function is linked with hyposecretion and lymphocytic infiltration in salivary glands of Sjögren's syndrome

Cong, Xin,Zhang, Xue-Ming,Zhang, Yan,Wei, Tai,He, Qi-Hua,Zhang, Li-Wei,Hua, Hong,Lee, Sang-Woo,Park, Kyungpyo,Yu, Guang-Yan,Wu, Li-Ling Elsevier 2018 Biochimica et biophysica acta. Molecular basis of Vol.1864 No.10

<P><B>Abstract</B></P> <P>Sjögren's syndrome (SS) is an inflammatory autoimmune disease that causes hyposecretion in salivary glands. Endothelial tight junctions (TJs) play crucial roles in salivation and barrier function of blood vessels. However, whether the alteration of endothelial TJs were involved in pathogenesis of SS was still unknown. Here, the ultrastructure and function of endothelial TJs in submandibular glands (SMGs) were detected by transmission electron microscopy and in vivo paracellular permeability assay in different aged NOD mouse model for SS. CFSE-labeled lymphocytes were injected into tail vein to trace the infiltration, while claudin-5 expression and distribution were detected by immunofluorescence, qRT-PCR, and western blot. Results showed that the stimulated salivary flow rate was gradually decreased and lymphocytic infiltration was found as age increased in 12- and 21-week-old NOD mice, but not 7-week-old NOD mice. Blood vessels were dilated, while endothelial TJ width and paracellular tracer transport were increased in 12-week-old NOD mice. Moreover, the injected CFSE-labeled lymphocytes were observed in SMGs of 12-week-old NOD mice. Claudin-5 level was increased and relocalized from the apical portion of neighboring endothelial cells to lateral membranes and cytoplasm in 12-week-old NOD mice. Additionally, the alteration of claudin-5 expression and distribution was further confirmed in labial salivary glands and bilateral parotid glands from SS patients. In cultured human microvessel endothelial cell line (HMEC-1), IFN-γ stimulation significantly increased claudin-5 expression. Taken together, we identified that the endothelial TJ barrier was disrupted and contributed to the development of salivary hyposecretion and lymphocytic infiltration in SS.</P> <P><B>Highlights</B></P> <P> <UL> <LI> Endothelial tight junction barrier is disrupted in hyposecretory submandibular glands from Sjögren's syndrome mouse model </LI> <LI> The disrupted salivary endothelial barrier is linked with lymphocytic infiltration in Sjögren's syndrome mouse model </LI> <LI> The redistribution of claudin-5 is responsible for disrupted endothelial barrier in salivary glands from Sjögren's syndrome </LI> </UL> </P>

p₂₂phox C₂₄₂T gene polymorphism and overt diabetic nephropathy: a meta-analysis of 1,452 participants

( Yan-yan Li ),( Ge Gong ),( Hong-yu Geng ),( Yun Qian ) 대한내과학회 2017 The Korean Journal of Internal Medicine Vol.32 No.6

Background/Aims: The p22phox C242T gene polymorphism (rs4673) may be linked to an increased susceptibility for overt diabetic nephropathy (ODN), but the study results are still inconclusive. Methods: To explore the relationship between p22phox C242T gene polymorphism and ODN, the current meta-analysis of 707 ODN patients and 745 controls from five individual studies was conducted. The pooled odds ratio (OR) and its corresponding 95% confidence interval (CI) were evaluated by either a random or fixed effect model. Results: In our meta-analysis, a significant relationship between the p22phox C242T gene polymorphism and ODN was found under allelic (OR, 2.760; 95% CI, 1.400 to 5.450; p = 0.004), recessive (OR, 5.080; 95% CI, 1.020 to 25.430; p = 0.05), dominant (OR, 1.700; 95% CI, 1.167 to 2.477; p = 0.006), homozygous (OR, 3.900; 95% CI, 1.022 to 14.889; p = 0.046), heterozygous (OR, 1.523; 95% CI, 1.167 to 1.986; p = 0.002), and additive genetic models (OR, 2.019; 95% CI, 1.232 to 3.309; p = 0.005). Conclusions: A positive correlation between p22phox C242T gene polymorphism and ODN risk was found. The T allele carriers of p22phox C242T gene polymorphism might be predisposed to ODN.

Two new sesquiterpenoids from endophytic fungus J3 isolated from Mangrove Plant Ceriops tagal

Yan-Bo Zeng,Hai-Gang Gu,Wen-Jian Zuo,Li-Li Zhang,Hong-Jin Bai,Zhi-Kai Guo,Peter Proksch,Wen Li Mei,Hao Fu Dai 대한약학회 2015 Archives of Pharmacal Research Vol.38 No.5

Two new sesquiterpenoids, named 2a-hydroxyxylaranolB (1) and 4b-hydroxyxylaranol B (2), togetherwith a known diterpenoid 3,4-seco-sonderianol (3) wereisolated from the fermentation of endophytic fungus J3 ofCeriops tagal. Their structures were elucidated based onspectroscopic methods including 1D and 2D NMR(HMQC, 1H-1H COSY and HMBC). All compounds wereevaluated for their cytotoxic activities by MTT method,and compound 3 exhibited cytotoxic activities againstK562, SGC-7901, and BEL-7402 cell lines.

Astilbin alleviates sepsis-induced acute lung injury by inhibiting the expression of macrophage inhibitory factor in rats

Hong-bo Zhang,Li-chao Sun,Li-da Zhi,Qian-kuan Wen,Zhi-wei Qi,Sheng-tao Yan,Wen Li,Guo-qiang Zhang 대한약학회 2017 Archives of Pharmacal Research Vol.40 No.10

Sepsis is a systemic inflammatory responsesyndrome caused by severe infections. Astilbin is a dihydroflavonolderivative found in many medicinal and foodplants with multiple pharmacological functions. To investigatethe effects of astilbin on sepsis-induced acute lunginjury (ALI), cecal ligation and puncture was performed onrats to establish a sepsis-induced ALI model; these ratswere then treated with astilbin at different concentrations. Lung injury scores, including lung wet/dry ratio, proteinleakage, myeloperoxidase activity, and inflammatory cellinfiltration were determined to evaluate the effects ofastilbin on sepsis-induced ALI. We found that astilbintreatment significantly attenuates sepsis-induced lunginjury and improves survival rate, lung injury scores, lungwet/dry ratio, protein leakage, myeloperoxidase activity,and inflammatory cell infiltration. Astilbin treatment alsodramatically decreased the production of inflammatorycytokines and chemokines in bronchoalveolar lavage fluid. Further, astilbin treatment inhibited the expression andproduction of macrophage inhibitory factor (MIF), whichinhibits the inflammatory response. Collectively, these datasuggest that astilbin has a protective effect against sepsisinducedALI by inhibiting MIF-mediated inflammatoryresponses. This study provides a molecular basis for astilbinas a new medical treatment for sepsis-induced ALI.

Sensory involvement in the SOD1-G93A mouse model of amyotrophic lateral sclerosis

Yan-Su Guo,Dong-Xia Wu,Hong-Ran Wu,Shu-Yu Wu,Cheng Yang,Bin Li,Hui Bu,Yue-sheng Zhang,Chun-Yan Li 생화학분자생물학회 2009 Experimental and molecular medicine Vol.41 No.3

A subset of patients of amyotrophic lateral sclerosis (ALS) present with mutation of Cu/Zn superoxide dismutase 1 (SOD1), and such mutants caused an ALSlike disorder when expressed in rodents. These findings implicated SOD1 in ALS pathogenesis and made the transgenic animals a widely used ALS model. However, previous studies of these animals have focused largely on motor neuron damage. We report herein that the spinal cords of mice expressing a human SOD1 mutant (hSOD1-G93A), besides showing typical destruction of motor neurons and axons, exhibit significant damage in the sensory system, including Wallerian-like degeneration in axons of dorsal root and dorsal funiculus, and mitochondrial damage in dorsal root ganglia neurons. Thus, hSOD1-G93A mutation causes both motor and sensory neuropathies, and as such the disease developed in the transgenic mice very closely resembles human ALS. A subset of patients of amyotrophic lateral sclerosis (ALS) present with mutation of Cu/Zn superoxide dismutase 1 (SOD1), and such mutants caused an ALSlike disorder when expressed in rodents. These findings implicated SOD1 in ALS pathogenesis and made the transgenic animals a widely used ALS model. However, previous studies of these animals have focused largely on motor neuron damage. We report herein that the spinal cords of mice expressing a human SOD1 mutant (hSOD1-G93A), besides showing typical destruction of motor neurons and axons, exhibit significant damage in the sensory system, including Wallerian-like degeneration in axons of dorsal root and dorsal funiculus, and mitochondrial damage in dorsal root ganglia neurons. Thus, hSOD1-G93A mutation causes both motor and sensory neuropathies, and as such the disease developed in the transgenic mice very closely resembles human ALS.