IL-13 R110Q, a Naturally Occurring IL-13 Polymorphism, Confers Enhanced Functional Activity in Cultured Human Bronchial Smooth Muscle Cells

Ya-fang He,Li Hua,Yi-xiao Bao,Quan-hua Liu,Yi Chu,Ding-zhu Fang 대한천식알레르기학회 2013 Allergy, Asthma & Immunology Research Vol.5 No.6

Purpose: Interleukin (IL)-13, a Th2-type cytokine, plays a pivotal role in the pathogenesis of asthma through its direct effects on airway smoothmuscles. A naturally occurring IL-13 polymorphism, R110Q, is strongly associated with increased total serum IgE levels and asthma. In the presentstudy, we aimed to determine whether the IL-13 R110Q variant would display different biochemical properties or altered functions in comparisonwith wild-type (WT) IL-13 in cultured human bronchial smooth muscle cells (hBSMCs). Methods: Culture supernatants and cell proteins were collectedfrom cultured hBSMCs that were treated with 50 ng/mL IL-13 or IL-13 R110Q for 24 h. Eotaxin released into hBSMC culture medium was determinedby ELISA. The expression levels of the high-affinity IgE receptor (FcεRI) α-chain, smooth muscle-specific actin alpha chain (α-SMA), smoothmuscle myosin heavy chain (SmMHC), and calreticulin in the cells were measured on Western blots. Results: Compared with WT IL-13, treatmentwith the IL-13 R110Q variant resulted in a significant increase in eotaxin release as well as significant, although modest, increases in the expressionlevels of α-SMA, SmMHC, calreticulin, and FcεRI α-chain. Conclusions: The results of the present study suggenst that the IL-13 R110Q variantmay enhance enhanced functional activities in hBSMCs.

Dietary inflammatory index and risk of gynecological cancers: a systematic review and meta-analysis of observational studies

Ze-ying Liu,Xu-ping Gao,Sui Zhu,Yan-hua Liu,Li-jun Wang,Chun-xia Jing,Fang-fang Zeng 대한부인종양학회 2019 Journal of Gynecologic Oncology Vol.30 No.3

Objective: There has been growing body of literatures showing that chronic inflammation might play an important role in cancer development. This meta-analysis aimed to assess the association between the dietary inflammation index (DII) score and gynecological cancers. Methods: A systematic search of PubMed, EMBASE and Web of Science up until October 20, 2018 was carried out to retrieve all related cohort and case-control studies. The summary risk assessments were pooled using random-effects models. The dose-response relationship was estimated by linear relationship model. Results: Twelve case-control studies (10,774 cases/15,958 controls) and six prospective cohort studies (330,363 participants/23,133 incident cases) were included in this meta-analysis. The pooled adjusted relative risk (RR) of gynecological cancers for the highest DII category compared to the lowest category was 1.38, (95% confidence intervals [CIs], 1.21–1.56, p<0.001]. A positive dose-response relationship was also noticed. Stratified by study design indicated that, the pooled RRs was significantly higher for case-control studies than cohort studies (p for interaction<0.001), for studies conducted among participants with body mass index (BMI) ≥25 kg/m2 than participants with BMI <25 kg/m2 (p for interaction=0.026), among participants with ovarian cancer and endometrial cancer than participants with breast cancer (p for interaction = 0.038). Meta-regression analysis further confirmed that study design significantly contributed to inter-study heterogeneity (p<0.001). Conclusion: This meta-analysis suggests that elevated DII is independently associated with a higher risk of gynecological cancers, especially patients with ovarian cancer and endometrial cancer and among obese participants.

RhGLP-1 (7-36) protects diabetic rats against cerebral ischemia-reperfusion injury via up-regulating expression of Nrf2/HO-1 and increasing the activities of SOD

Fang, Yi,Liu, Xiaofang,Zhao, Libo,Wei, Zhongna,Jiang, Daoli,Shao, Hua,Zang, Yannan,Xu, Jia,Wang, Qian,Liu, Yang,Peng, Ye,Yin, Xiaoxing The Korean Society of Pharmacology 2017 The Korean Journal of Physiology & Pharmacology Vol.21 No.5

The present study aimed to explore the neuroprotective effect and possible mechanisms of rhGLP-1 (7-36) against transient ischemia/reperfusion injuries induced by middle cerebral artery occlusion (MCAO) in type 2 diabetic rats. First, diabetic rats were established by a combination of a high-fat diet and low-dose streptozotocin (STZ) (30 mg/kg, intraperitoneally). Second, they were subjected to MCAO for 2 h, then treated with rhGLP-1 (7-36) (10, 20, $40{\mu}g/kg$ i.p.) at the same time of reperfusion. In the following 3 days, they were injected with rhGLP-1 (7-36) at the same dose and route for three times each day. After 72 h, hypoglycemic effects were assessed by blood glucose changes, and neuroprotective effects were evaluated by neurological deficits, infarct volume and histomorphology. Mechanisms were investigated by detecting the distribution and expression of the nuclear factor erythroid-derived factor 2 related factor 2 (Nrf2) in ischemic brain tissue, the levels of phospho-PI3 kinase (PI3K)/PI3K ratio and heme-oxygenase-1 (HO-l), as well as the activities of superoxide dismutase (SOD) and the contents of malondialdehyde (MDA). Our results showed that rhGLP-1 (7-36) significantly reduced blood glucose and infarction volume, alleviated neurological deficits, enhanced the density of surviving neurons and vascular proliferation. The nuclear positive cells ratio and expression of Nrf2, the levels of P-PI3K/PI3K ratio and HO-l increased, the activities of SOD increased and the contents of MDA decreased. The current results indicated the protective effect of rhGLP-1 (7-36) in diabetic rats following MCAO/R that may be concerned with reducing blood glucose, up-regulating expression of Nrf2/HO-1 and increasing the activities of SOD.

Hydrogen sulfide inhibits the growth of Escherichia coli through oxidative damage

Liu-Hui Fu,Zeng-Zheng Wei,Kang-Di Hu,Lan-Ying Hu,Yan-Hong Li,Xiao-Yan Chen,Zhuo Han,Gai-Fang Yao,Hua Zhang 한국미생물학회 2018 The journal of microbiology Vol.56 No.4

Many studies have shown that hydrogen sulfide (H2S) is both detrimental and beneficial to animals and plants, whereas its effect on bacteria is not fully understood. Here, we report that H2S, released by sodium hydrosulfide (NaHS), significantly inhibits the growth of Escherichia coli in a dose-dependent manner. Further studies have shown that H2S treatment stimulates the production of reactive oxygen species (ROS) and decreases glutathione (GSH) levels in E. coli, resulting in lipid peroxidation and DNA damage. H2S also inhibits the antioxidative enzyme activities of superoxide dismutase (SOD), catalase (CAT) and glutathione reductase (GR) and induces the response of the SoxRS and OxyR regulons in E. coli. Moreover, pretreatment with the antioxidant ascorbic acid (AsA) could effectively prevent H2S-induced toxicity in E. coli. Taken together, our results indicate that H2S exhibits an antibacterial effect on E. coli through oxidative damage and suggest a possible application for H2S in water and food processing.

INTERACTIONS OF THE INFRARED BUBBLE N4 WITH ITS SURROUNDINGS

Liu, Hong-Li,Li, Jin-Zeng,Wu, Yuefang,Yuan, Jing-Hua,Liu, Tie,Dubner, G.,Paron, S.,Ortega, M. E.,Molinari, Sergio,Huang, Maohai,Zavagno, Annie,Samal, Manash R.,Huang, Ya-Fang,Zhang, Si-Ju American Astronomical Society 2016 The Astrophysical journal Vol.818 No.1

<P>The physical mechanisms that induce the transformation of a certain mass of gas in new stars are far from being well understood. Infrared bubbles associated with H II regions have been considered to be good samples for investigating triggered star formation. In this paper we report on the investigation of the dust properties of the infrared bubble N4 around the H II. region G11.898+0.747, analyzing its interaction with its surroundings and star formation histories therein, with the aim of determining the possibility of star formation triggered by the expansion of the bubble. Using Herschel PACS and SPIRE images with a wide wavelength coverage, we reveal the dust properties over the entire bubble. Meanwhile, we are able to identify six dust clumps surrounding the bubble, with a mean size of 0.50 pc, temperature of about 22 K, mean column density of 1.7 x 10(22) cm(-2), mean volume density of about 4.4 x 10(4) cm(-3), and a mean mass of 320M(circle dot). In addition, from PAH emission seen at 8 mu m, free-free emission detected at 20 cm, and a probability density function in special regions, we could identify clear signatures of the influence of the H II region on the surroundings. There are hints of star formation, though further investigation is required to demonstrate that N4 is the triggering source.</P>

Glucosamine induces cell death $via$ proteasome inhibition in human ALVA41 prostate cancer cell

Liu, Bao-Qin,Meng, Xin,Li, Chao,Gao, Yan-Yan,Li, Ning,Niu, Xiao-Fang,Guan, Yifu,Wang, Hua-Qin Korean Society for Biochemistry and Molecular Bion 2011 Experimental and molecular medicine Vol.43 No.9

Glucosamine, a naturally occurring amino monosaccharide, has been reported to play a role in the regulation of apoptosis more than half century. However the effect of glucosamine on tumor cells and the involved molecular mechanisms have not been thoroughly investigated. Glucosamine enters the hexosamine biosynthetic pathway (HBP) downstream of the rate-limiting step catalyzed by the GFAT (glutamine:fluctose- 6-phosphate amidotransferase), providing UDP-GlcNAc substrates for O-linked ${\beta}$-N-acetylglucosamine (O-GlcNAc) protein modification. Considering that O-GlcNAc modification of proteasome subunits inhibits its activity, we examined whether glucosamine induces growth inhibition $via$ affecting proteasomal activity. In the present study, we found glucosamine inhibited proteasomal activity and the proliferation of ALVA41 prostate cancer cells. The inhibition of proteasomal activity results in the accumulation of ubiquitinated proteins, followed by induction of apoptosis. In addition, we demonstrated that glucosamine downregulated proteasome activator $PA28{\gamma}$ and overexpression of $PA28{\gamma}$ rescued the proteasomal activity and growth inhibition mediated by glucosamine. We further demonstrated that inhibition of O-GlcNAc abrogated $PA28{\gamma}$ suppression induced by glucosamine. These findings suggest that glucosamine may inhibit growth of ALVA41 cancer cells through downregulation of $PA28{\gamma}$ and inhibition of proteasomal activity via O-GlcNAc modification.

Aberrant Expression of CCAT1 Regulated by c-Myc Predicts the Prognosis of Hepatocellular Carcinoma

Zhu, Hua-Qiang,Zhou, Xu,Chang, Hong,Li, Hong-Guang,Liu, Fang-Feng,Ma, Chao-Qun,Lu, Jun Asian Pacific Journal of Cancer Prevention 2015 Asian Pacific journal of cancer prevention Vol.16 No.13

Background: CCAT1 has been reported to be linked with pathogenesis of malignancies including colon cancer and gastric cancer. However, the regulatory effect of CCAT1 in hepatocellular carcinoma (HCC) remains unclear. The purpose of this research was to identify any role of CCAT1 in the progression of HCC. Materials and Methods: Real time-PCR was performed to test the relative expression of CCAT1 in HCC tissues. A computation screen of CCAT1 promoter was conducted to search for transcription-factor-binding sites. The association of c-Myc with CCAT1 promoter in vivo was tested by Pearson correlation analysis and chromatin immunoprecipitation assay. Additionally, Kaplan-Meier analysis and Cox proportional hazards analyses were performed. Results: c-Myc directly binds to the E-box element in the promoter region of CCAT, and when ectopically expressed increases promoter activity and expression of CCAT1. Moreover, Kaplan-Meier analysis demonstrated that the patients with low expression of CCAT1 demonstrated better overall and relapse-free survival compared with the high expression group. Cox proportional hazards analyses showed that CCAT1 expression was an independent prognostic factor for HCC patients. Conclusions: The findings demonstrated CCAT1, acting as a potential biomarker in predicting the prognosis of HCC, is regulated by c-Myc.

Single-cell RNA sequencing reveals B cell–related molecular biomarkers for Alzheimer’s disease

Xiong Liu-Lin,Xue Lu-Lu,Du Ruo-Lan,Niu Rui-Ze,Chen Li,Chen Jie,Hu Qiao,Tan Ya-Xin,Shang Hui-Fang,Liu Jia,Yu Chang-Yin,Wang Ting-Hua 생화학분자생물학회 2021 Experimental and molecular medicine Vol.53 No.-

In recent years, biomarkers have been integrated into the diagnostic process and have become increasingly indispensable for obtaining knowledge of the neurodegenerative processes in Alzheimer’s disease (AD). Peripheral blood mononuclear cells (PBMCs) in human blood have been reported to participate in a variety of neurodegenerative activities. Here, a single-cell RNA sequencing analysis of PBMCs from 4 AD patients (2 in the early stage, 2 in the late stage) and 2 normal controls was performed to explore the differential cell subpopulations in PBMCs of AD patients. A significant decrease in B cells was detected in the blood of AD patients. Furthermore, we further examined PBMCs from 43 AD patients and 41 normal subjects by fluorescence activated cell sorting (FACS), and combined with correlation analysis, we found that the reduction in B cells was closely correlated with the patients’ Clinical Dementia Rating (CDR) scores. To confirm the role of B cells in AD progression, functional experiments were performed in early-stage AD mice in which fibrous plaques were beginning to appear; the results demonstrated that B cell depletion in the early stage of AD markedly accelerated and aggravated cognitive dysfunction and augmented the Aβ burden in AD mice. Importantly, the experiments revealed 18 genes that were specifically upregulated and 7 genes that were specifically downregulated in B cells as the disease progressed, and several of these genes exhibited close correlation with AD. These findings identified possible B cell-based AD severity, which are anticipated to be conducive to the clinical identification of AD progression.

Rapid preparation and characterization of chitosan nanoparticles for oligonucleotide

Mu-hua Cheng,Yao-xiong Huang,Han-jian Zhou,Zhi Liu,Jian-fang Li 한국물리학회 2010 Current Applied Physics Vol.10 No.3

Chitosan is regarded as one of the potential candidates as a gene carrier. However, the poor solubility of chitosan is the major limiting factor in its utilization as a gene carrier. The purpose of this study was to simplify the method of preparing the nanoparticles of chitosan linked with antisense oligonucleotide (asON). The main step was preparing the derivatives of chitosan phosphate (CSP) in order to easily dissolve in aqueous solution. The nanoparticles were formed using a simple mixed method for CSP and asON, and the nanoparticle’s forming condition was optimized so that the nanoparticle’s characterization could be examined. Results showed that it was simple to make the nanoparticles under the optimal condition of 2:1 M proportion of CSP and asON. The size of the nanoparticles was 102.6 ± 12.0 nm, its zeta potential was 1.45 ± 1.75, and the encapsulated ratio of the chitosan crosslinked the asON was 87.6 ± 3.5%. The infrared spectra and electron microscope displayed that chitosan may combine with the asON to form equirotal nanoparticles. In conclusion, it was simple and feasible to form chitosan nanoparticles for asON using the CSP, and the CSP can efficiently encapsulate asON.

RhGLP-1 (7-36) protects diabetic rats against cerebral ischemia-reperfusion injury via up-regulating expression of Nrf2/HO-1 and increasing the activities of SOD

Yi Fang,Xiaofang Liu,Libo Zhao,Zhongna Wei,Daoli Jiang,Hua Shao,Yannan Zang,Jia Xu,Qian Wang,Yang Liu,Ye Peng,Xiaoxing Yin 대한약리학회 2017 The Korean Journal of Physiology & Pharmacology Vol.21 No.5

The present study aimed to explore the neuroprotective effect and possible mechanisms of rhGLP-1 (7-36) against transient ischemia/reperfusion injuries induced by middle cerebral artery occlusion (MCAO) in type 2 diabetic rats. First, diabetic rats were established by a combination of a high-fat diet and low-dose streptozotocin (STZ) (30 mg/kg, intraperitoneally). Second, they were subjected to MCAO for 2 h, then treated with rhGLP-1 (7-36) (10, 20, 40 μg/kg i.p.) at the same time of reperfusion. In the following 3 days, they were injected with rhGLP-1 (7- 36) at the same dose and route for three times each day. After 72 h, hypoglycemic effects were assessed by blood glucose changes, and neuroprotective effects were evaluated by neurological deficits, infarct volume and histomorphology. Mechanisms were investigated by detecting the distribution and expression of the nuclear factor erythroid-derived factor 2 related factor 2 (Nrf2) in ischemic brain tissue, the levels of phospho-PI3 kinase (PI3K)/PI3K ratio and heme-oxygenase-1 (HO-l), as well as the activities of superoxide dismutase (SOD) and the contents of malondialdehyde (MDA). Our results showed that rhGLP-1 (7-36) significantly reduced blood glucose and infarction volume, alleviated neurological deficits, enhanced the density of surviving neurons and vascular proliferation. The nuclear positive cells ratio and expression of Nrf2, the levels of P-PI3K/PI3K ratio and HO-l increased, the activities of SOD increased and the contents of MDA decreased. The current results indicated the protective effect of rhGLP-1 (7-36) in diabetic rats following MCAO/R that may be concerned with reducing blood glucose, up-regulating expression of Nrf2/HO-1 and increasing the activities of SOD.