Zhongdong Qiao

Shanghai University, Shanghai, Shanghai Shi, China

Are you Zhongdong Qiao?

Claim your profile

Publications (29)89.11 Total impact

  • J. Dai · C. Zhan · W. Xu · Z. Wang · D. Nie · X. Zhao · D. Zhang · Y. Gu · L. Wang · Z. Chen · Z. Qiao
    [Show abstract] [Hide abstract]
    ABSTRACT: Many studies have addressed the hazardous role of cigarette smoking on male fertility, but the exact molecular mechanisms involved in the impairments caused by nicotine remain unclear. To evaluate the detrimental effects of nicotine exposure on spermatogenesis, two-dimensional gel electrophoresis and mass spectrometry analysis were performed to screen and identify differentially expressed proteins from the testes of mice exposed to nicotine daily. Data mining analysis indicated that the 15 identified proteins were mainly involved in actin cytoskeleton regulation and in the tricarboxylic acid cycle, which are related to cell motility. Further investigation of a central regulatory factor in the cytoskeleton regulation, profilin 1 (PFN1), revealed that nicotine-induced Pfn1 over-expression in mouse testes, specifically in elongated spermatids, by Pfn1 promoter hypomethylation. Interestingly, elevated sperm motility parameters were observed in nicotine-treated mice. We assume that nicotine-induced PFN1 over-expression in mouse spermatids may promote actin polymerization and ultimately enhance sperm motility. © 2015 American Society of Andrology and European Academy of Andrology.
    Andrology 09/2015; 3(5). DOI:10.1111/andr.12072 · 3.37 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Cigarette smoking is associated with lower semen quality, but how cigarette smoking changes the semen quality remains unclear. The aim of this study was to screen the differentially expressed proteins in the sperm of mice with daily exposure to cigarette smoke. The 2D gel electrophoresis (2DE) and mass spectrometry (MS) analyses results showed that the mouse sperm protein profile was altered by cigarette smoking. And 22 of the most abundant proteins that correspond to differentially expressed spots in 2DE gels of the sperm samples were identified. These proteins were classified into different groups based on their functions, such as energy metabolism, reproduction, and structural molecules. Furthermore, the 2DE and MS results of five proteins (Aldoa, ATP5a1, Gpx4, Cs, and Spatc1) were validated by western blot analysis and reverse transcriptase-polymerase chain reaction. Results showed that except Spatc1 the other four proteins showed statistically significant different protein levels between the smoking group and the control group (P < 0.05). The expressions of three genes (Aldoa, Gpx4, and Spatc1) were significantly different (P < 0.05) at transcription level between the smoking group and the control group. In addition, five proteins (Aldoa, ATP5a1, Spatc1, Cs, and Gpx4) in human sperm samples from 30 male smokers and 30 non-smokers were detected by western blot analysis. Two proteins (Aldoa and Cs) that are associated with energy production were found to be significantly altered, suggesting that these proteins may be potential diagnostic markers for evaluation of smoking risk in sperm. Further study of these proteins may provide insight into the pathogenic mechanisms underlying infertility in smoking persons.
    Acta Biochimica et Biophysica Sinica 07/2015; 47(7). DOI:10.1093/abbs/gmv045 · 2.09 Impact Factor
  • Weiwei Qi · Jianying Niu · Qiaojing Qin · Zhongdong Qiao · Yong Gu
    [Show abstract] [Hide abstract]
    ABSTRACT: Glycated albumin (GA), an Amadori product used as a marker of hyperglycemia and the early-stage glycation products compared to AGEs, might further promote kidney lesions in diabetic nephropathy (DN). However, the mechanisms how GA cause proximal tubular cells damage remain poorly understood. In this study, we investigated the effects of GA on fibrosis and apoptosis of renal proximal tubular cells (NRK-52E) in vitro experiments. Our results showed that GA promoted α-SMA, fibronectin (FN) and TGF-β expressions in NRK-52E cells. GA also increased cell apoptosis and stimulated the expressions of pro-caspase 3/cleaved-caspase 3. GA overloading enhanced the phosphorylation of MAPK pathway. GA-induced α-SMA, FN, TGF-β and caspase 3 expressions were completely suppressed by the NADPH oxidase inhibitor apocynin (Apo), the reactive oxygen species (ROS) scavenger N-acetylcysteine (NAC) and the latent antioxidant Astragaloside IV (AS-IV). Real-time PCR showed that GA increased Nox1, Nox2 and Nox4 mRNA expressions, especially the Nox4 expression. Furthermore, Nox4 siRNA blocked GA-induced tubular damages and the MAPK pathway activation. These results demonstrate that GA increases the permissiveness of proximal tubular cells to fibrosis and apoptosis in vitro by triggering a pathway that involves NADPH oxidase/Nox4-MAPK signaling pathway. This event may represent a key cellular effect in increasing the susceptibility of tubular cells to fibrosis and apoptosis when the tubules cope with a high GA load. This effect is instrumental to renal damage and disease progression in patients with DN.
    Molecular and Cellular Endocrinology 02/2015; 405. DOI:10.1016/j.mce.2015.02.007 · 4.24 Impact Factor
  • P. Fang · W. Xu · D. Li · X. Zhao · J. Dai · Z. Wang · X. Yan · M. Qin · Y. Zhang · C. Xu · L. Wang · Z. Qiao
    [Show abstract] [Hide abstract]
    ABSTRACT: On the basis of the unknown tags in the mature human sperm serial analysis of gene expression library constructed by our laboratory, some transcripts were cloned, including Iqcf1 (IQ motif containing F1). To investigate the function of sperm-retained Iqcf1 in spermatogenesis and fertilization of mice, we investigated the spatial and temporal expression of IQCF1. By using the (transcription activator-like effector nuclease) strategy, Iqcf1-knockout mice were produced, and the phenotypes of the Iqcf1−/− mice were analyzed. The results showed that IQCF1 was localized in the acrosome of spermatozoa and spermatids; the expression of IQCF1 in testes was associated with spermatogenic capacity. The Iqcf1−/− mice were significantly less fertile than the wild-type mice (p = 0.0057) because of reduced sperm motility (p = 0.0094) and the acrosome reaction (AR) (p = 0.0093). In spermatozoa, IQCF1 interacted with calmodulin (CaM) and possibly participated in the tyrosine phosphorylation of sperm proteins during capacitation. In conclusion, a newly identified acrosomal protein, IQCF1, is closely related to sperm capacitation and AR; in particular, it is involved in tyrosine phosphorylation of sperm proteins through interaction with CaM. Research into the function of IQCF1 during fertilization could facilitate the investigation of the molecular mechanism of capacitation, which is unclear.
    Andrology 10/2014; 3(2). DOI:10.1111/andr.296 · 3.37 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: The underlying mechanisms of proteinuria, a main characteristic of preeclampsia (PE), have not yet been fully elucidated. Evidence indicates that the renin-angiotensin system (RAS) is involved in the pathogenesis of this disease, including decreased angiotensin-(1-7) [Ang-(1-7)] levels in the circulation and urine. In the present study, we examined the damage to podocytes induced by preeclamptic serum and the effects of Ang-(1-7) on podocytes treated with preeclamptic serum, as well as the underlying mechanisms. The podocytes were incubated with serum obtained from women with PE or with serum from women with normal pregnancies for different periods of time. Cell viability was determined by CCK-8 assay. The cells were treated with various concentrations of Ang-(1-7) and A779 [an (Ang-(1-7) antagonist]. The effects of Ang-(1-7) on the expression of podocyte-specific proteins [nephrin, Wilms tumor‑1 (WT-1) and podocin] and the phosphorylation of mitogen-activated protein kinases (MAPKs) were investigated by western blot analysis. Changes in F-actin rearrangement were determined by immunofluorescence. Podocyte apoptosis was determined by flow cytometry. The results revealed that in the cultured podocytes incubated with preeclamptic serum, there was a decrease in the expression of podocyte-specific proteins (nephrin and WT-1 but not podocin), a rearrangement of F-actin and apoptosis compared with the control group. However, treatment with Ang-(1-7) attenuated podocyte injury in the preeclamptic group, which may be mediated through the downregulation of MAPK (p38, ERK1/2 and JNK) phosphorylation. Thus, our data suggest that Ang-(1-7) plays a protective role in PE through the downregulation of MAPK phosphorylation.
    International Journal of Molecular Medicine 07/2014; 34(4). DOI:10.3892/ijmm.2014.1870 · 1.88 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Microglia, the main immune cells of the central nervous system (CNS), play a vital role in the development of AD. Once microglia are activated, they migrate to neuritic plaques and persistently release pro-inflammatory mediators that lead to neuroinflammation and neuronal degeneration, accelerating the progression of AD. In this study, we analyzed whether an AD candidate drug, N-[2-(3,4-dimethoxyphenyl)ethyl]-3-phenyl-acrylamide (gx-50), a compound extracted from Sichuan pepper (Zanthoxylum bungeanum), exhibited suppressive effects on the chemotactic migration of microglia induced by Aβ. At first, the effects of gx-50 on the migration of primary cultured microglia to Aβ were detected by transwell assay, and the secretion of chemokine CCL5 was measured by ELISA assay. Then, the release of TGF-β1 was detected by ELISA and quantitative real-time PCR, and the activation of the TGF-β1-Smad2 pathway was analyzed by Western blotting. The LDH assay revealed that cell viability was not affected by gx-50 at concentrations from 0.01 to 100 μM; thus, combined with our previous studies, 1 μM was chosen as the treatment concentration. The cell transwell measurement demonstrated that gx-50 suppressed the chemotactic migration of microglia by nearly 50% and inhibited the increase in CCL5 triggered by Aβ. Moreover, the analysis of the TGF-β1-Smad2 pathway revealed that gx-50 can antagonize Aβ-induced down-regulation of TGF-β1 at both the mRNA and protein levels and stimulate the signal pathway activation. Simultaneously, gx-50 pretreatment also significantly enhanced the phosphorylation of glycogen synthase kinase-3β (GSK-3β), which correlated closely with the migration of microglia. In conclusion, in the presence of Aβ, gx-50 pretreatment inhibited the excessive chemotactic migration of microglia.
    International immunopharmacology 04/2014; 19(2). DOI:10.1016/j.intimp.2014.01.025 · 2.71 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: To study the diversity of mRNAs in murine spermatozoa and their potential function during zygotic development, the total RNAs in murine spermatozoa were sequenced via RNA-Seq and analyzed through bioinformatics techniques. The delivery and translation of sperm-borne mRNA in fertilized oocyte were detected using RT-PCR (reverse transcription-polymerase chain reaction), Western blotting, and immunofluorescence. A total of 35,288,825 reads matching 33,039 transcripts, including 27,310 coding transcripts, were obtained. Based on our analyses, we hypothesized that the transcripts with RPKM (reads per kilobase of exon model per million mapped reads) higher than 6 may exist in each sperm cell as consistently retained transcripts. There were 4,885 consistent transcripts in each sperm, and the remainder were randomly retained. If the baseline RPKM increased, the remained coding transcripts were more likely related to reproduction and development. The sperm-borne transcripts Wnt4 and Foxg1 were delivered into fertilized oocytes upon fertilization. Furthermore, Wnt4 was translated into protein in zygotes, whereas Foxg1 was not translated. In conclusion, approximately 4,885 mRNAs were present in each murine spermatozoon, and the spermatozoal mRNAs related to reproduction and development were more likely retained. The sperm-borne mRNAs Wnt4 was delivered into the fertilized oocyte and translated, as an evidence of paternal effect on zygotic development.
    Biology of Reproduction 03/2014; 90(5). DOI:10.1095/biolreprod.114.117788 · 3.45 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Aggregation of amyloid-beta (Aβ) fragments is one of the major pathological hallmarks of Alzheimer's disease (AD). Our previous study has demonstrated that a novel compound named N-[2-(3, 4-dimethoxyphenyl) ethyl]-3-phenyl-acrylamide (gx-50) can decrease the accumulation of Aβ oligomers in the cerebral cortex and improve the cognitive abilities in transgenic demented mice. To further study the mechanism of the neuroprotective effect of gx-50 against AD, we employed microarray to investigate the gene expression profile of the primary cultured neurons treated with gx-50 or/and Aβ. Microarray disclosed 351 genes associated with AD in the gx-50 plus Aβ treated group, out of the 22523 probes. 217 of the 351 genes were significantly up-regulated, 134 of them were down-regulated. The 351 genes were mainly involved in neurotransmission, signal transduction, nervous system development, protein phosphorylation, transcription and apoptosis. By the Onto-pathway analysis, a network involved two molecules - GSK-3, CREB and another two closely linked proteins - AKT, BDNF was discovered. The GSK/CREB pathway was further studied at the gene and protein level both in vivo and in vitro. Western blot and immunohistochemistry analysis showed that the gx-50 elevated the AKT phosphorylation and inhibited its downstream protein - GSK-3's activity, then restored the CREB's transcriptional activity, and finally enhanced the expression of the CREB target gene - BDNF. In addition, the real-time PCR results displayed the same tendency. In conclusion, studies in this research indicated that the gx-50 may improve the cognitive ability of AD via the GSK-3/CREB pathway.
    Neuropharmacology 02/2014; 81. DOI:10.1016/j.neuropharm.2014.02.008 · 4.82 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Many studies have addressed the role of cigarette smoking on semen quality, but the exact mechanisms remain inconclusive. To evaluate the detrimental effects of smoking on the spermatogenesis process, we initially screened and investigated 31 differentially expressed proteins extracted from the testes of mice exposed daily to cigarette smoke using MALDI-TOF-MS analysis. Data mining analysis showed that these 31 proteins were categorised into five functional clustering groups: metabolic process, cell growth and/or maintenance, RNA and protein processing, stress response and spermatogenesis. Additionally, 23 of 31 proteins are involved in a main pathway network, including Pkc (s), ERK1/2, Akt, and NF-κB, which are known to be involved in cell communication, proliferation and differentiation. Interestingly, among the 31 proteins, a spermatogenesis-associated protein, phosphatidylethanolamine-binding protein 1 (PEBP1), is especially expressed in serial sections of spermatids of spermiogenesis and interacts with ERKs. Bisulphite sequencing result shows four CpGs near Pebp1 transcriptional start site are largely methylated in the treated group. 5-aza-2'-deoxycytidine treatment on GC-1 spg cells reverses the hypermethylation status and elevates both Pebp1 mRNA and protein expression levels. ERK1/2 phosphorylation levels are also increased with upregulation of Pebp1 expression in GC-1 spg cells. In conclusion, protein profile in testes could be altered by cigarette smoking. Moreover, we also suggest that epigenetical Pebp1 inactivation may affect activation of ERK, and it could impair spermatogenesis of mice. Our data could provide further insight into the mechanisms of spermatogenesis.
    Biology of Reproduction 11/2013; 89(6). DOI:10.1095/biolreprod.113.111245 · 3.45 Impact Factor
  • Zhaoxia Wang · Wangjie Xu · Xiuwen Zhao · Peng Fang · Lianyun Wang · Zhongdong Qiao
    Acta Biochimica et Biophysica Sinica 06/2013; 45(9). DOI:10.1093/abbs/gmt068 · 2.09 Impact Factor
  • Weiwei Qi · Jianying Niu · Qiaojing Qin · Zhongdong Qiao · Yong Gu
    [Show abstract] [Hide abstract]
    ABSTRACT: In diabetic kidney disease (DKD), epithelial-to-mesenchymal transition (EMT) is a classic pathological process in tubular damage. Oxidative stress is considered to play an important role in DKD. Astragaloside IV (A-IV), one of the main active ingredients of Astragalus membranaceus, exhibits a wide range of biological activities. However, the effect of A-IV on regulating EMT in tubular cells is unclear. This study aims to determine whether A-IV could attenuate glycated albumin (GA)-induced EMT in the NRK-52E cell line by inhibiting oxidative stress. GA and A-IV-induced cytotoxicity were assayed by CCK-8. The intercellular reactive oxygen species (ROS) level was detected by H2DCFDA. The activity of NADPH oxidase was assayed by adding exogenous NADPH oxidase, and the superoxide dismutase (SOD) units were observed by NBT. We used a microscope to examine the morphology of the NRK-52E cell line. We conducted a wound healing assay to measure cell mobility. To determine mRNA and protein expressions of α-SMA and E-cadherin, we used real-time polymerase chain reaction (real-time PCR), immunofluorescence, and western blot analysis. A-IV significantly attenuated GA-induced amplification of ROS, lowered the increased level of NADPH oxidase activity, and elevated the decreased level of SOD units. The GA-induced NRK-52E cell line showed increased expression of α-SMA and decreased expression of E-cadherin in mRNA and protein levels, whereas A-IV alleviated the expression of α-SMA and increased the expression of E-cadherin. Our data demonstrate that GA could induce NRK-52E cell line EMT through oxidative stress. This effect could be attenuated by A-IV via regulation of the impaired redox balance.
    Cell Stress and Chaperones 05/2013; 19(1). DOI:10.1007/s12192-013-0438-7 · 2.54 Impact Factor
  • Shi Shi · Zhaoxia Wang · Zhongdong Qiao
    [Show abstract] [Hide abstract]
    ABSTRACT: Inflammation has recently been implicated as a critical mechanism in Alzheimer's disease (AD). Microglia are the resident immune cells in the central nervous system (CNS), and they mediate the inflammatory response in the AD brain. Thus, suppression of microglial activation and subsequent neuroinflammation may be a potential therapeutic approach against AD. In the following review, we briefly discuss the limitations and advantages of current drug targets for AD and then summarize several anti-inflammatory drugs in trial, including natural nonsteroidal anti-inflammatory drugs (NSAIDs), polyphenols and new drugs synthesized based on multi-target directed ligand (MTDL) design. In addition to their anti-inflammatory effects, these drugs can act as anti-oxidants and reduce microglial activation or amyloid-β (Aβ) plaques. Thus, the studies focused on multiple factors in AD processes might reveal the best potential treatment strategy for the future.
    Current Medicinal Chemistry 04/2013; 20. DOI:10.2174/0929867311320200006 · 3.85 Impact Factor
  • Source
    Qiaojing Qin · Jianying Niu · Zhaoxia Wang · Wangjie Xu · Zhongdong Qiao · Yong Gu
    [Show abstract] [Hide abstract]
    ABSTRACT: Background Advanced glycation end products (AGEs), inflammatory-associated macrophage migration and accumulation are crucial for initiation and progression of diabetic vascular complication. Enzymatic activity of heparanase (HPA) is implicated strongly in dissemination of metastatic tumor cells and cells of the immune system. In addition, HPA enhances the phosphorylation of selected signaling molecules including AKT pathway independent of enzymatic activity. However, virtually nothing is presently known the role of HPA during macrophage migration exposed to AGEs involving signal pathway. Methods These studies were carried out in Ana-1 macrophages. Macrophage viability was measured by MTT (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide) assays. HPA and AKT protein expression in macrophages are analysed by Western blotting and HPA mRNA expression by real time quantitative RT-PCR. Release of HPA was determined by ELISA. Macrophage migration was assessed by Transwell assays. Results HPA protein and mRNA were found to be increased significantly in AGEs-treated macrophages. Pretreatment with anti-HPA antibody which recognizes the nonenzymatic terminal of HPA prevented AGEs-induced AKT phosphorylation and macrophage migration. LY294002 (PI3k/AKT inhibitor) inhibited AGEs-induced macrophage migration. Furthermore, pretreatment with anti-receptor for advanced glycation end products (RAGE) antibody attenuated AGEs-induced HPA expression, AKT phosphorylation and macrophage migration. Conclusions These data indicate that AGEs-induced macrophage migration is dependent on HPA involving RAGE-HPA-PI3K/AKT pathway. The nonenzymatic activity of HPA may play a key role in AGEs-induced macrophage migration associated with inflammation in diabetic vascular complication.
    Cardiovascular Diabetology 02/2013; 12(1):37. DOI:10.1186/1475-2840-12-37 · 3.71 Impact Factor
  • Source
    Qiaojing Qin · Jianying Niu · Zhaoxia Wang · Wangjie Xu · Zhongdong Qiao · Yong Gu
    [Show abstract] [Hide abstract]
    ABSTRACT: Advanced glycation end products (AGEs) and inflammation contribute to the development of diabetic complications. Astragalus membranaceus has properties of immunological regulation in many diseases. The aim of this study was to determine the function of A. membranaceus extract (AME) on the AGE-induced inflammatory response in Ana-1 macrophages. The viability of cells treated with AME or AGEs was evaluated with the MTT [3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2H-tetrazolium bromide] method. The secretion and mRNA levels of IL-1β and TNF-α were measured by ELISA and RT-PCR, respectively. The activity of NF-κB was assayed by EMSA. The phosphorylation of p38 MAPK was assessed by western blotting. The results showed that AME was not toxic to macrophages. The treatment of macrophages with AME effectively inhibited AGE-induced IL-1β and TNF-α secretion and mRNA expression in macrophages. These effects may be mediated by p38 MAPK and the NF-κB pathway. The results suggest that AME can inhibit AGE-induced inflammatory cytokine production to down-regulate macrophage-mediated inflammation via p38 MAPK and NF-κB signaling pathways and indicate that AME could be an immunoregulatory agent against AGE-induced inflammation in diabetes.
    International Journal of Molecular Sciences 12/2012; 13(7):8379-87. DOI:10.3390/ijms13078379 · 2.86 Impact Factor
  • Source
    Qiaojing Qin · Jianying Niu · Zhaoxia Wang · Wangjie Xu · Zhongdong Qiao · Yong Gu
    [Show abstract] [Hide abstract]
    ABSTRACT: Astragalus membranaceus (AM), a traditional Chinese medicinal herb, has immunoregulatory properties in many diseases. We investigated the effects and mechanism of Astragalus membranaceus extract (AME) in the macrophage migration and immune response mediator release. The viability of Ana-1 macrophages treated with AME was evaluated by the MTT method. The secretion and mRNA levels of IL-1β and TNF-a were measured by ELISA and RT-PCR, respectively. Macrophage migration was assayed by transwell assay. The activity of heparanase (HPA) was determined by a heparin-degrading enzyme assay. Our results didn't show any toxicity of AME in macrophages. AME increased the activity of HPA, cell migration, mRNA levels and secretion of IL-1β and TNF-a in macrophages. Pretreatment with anti-HPA antibody reduced cell migration, secretion of IL-1β and TNF-a did not change the mRNA levels of IL-1β and TNF-a significantly in AME-treated macrophages. This suggests that AME may increase the release of immune response mediator and cell migration via HPA to activate immune response in macrophages.
    Molecules 12/2012; 17(6):7232-40. DOI:10.3390/molecules17067232 · 2.42 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: This study focused on a promising drug candidate, N-[2-(3,4-dimethoxyphenyl)ethyl]-3-phenyl-acrylamide (gx-50), a compound extracted from Sichuan pepper (Zanthoxylum Bungeanum), to determine whether it would be an effective therapeutic for Alzheimer's disease (AD) via biological experiments. In vivo, we determined the pharmacokinetic profile of gx-50 and evaluated the effect of gx-50 on the cognitive abilities of amyloid-β protein precursor transgenic (AβPP-Tg) mice by Morris water maze testing. In addition, we examined the effects of gx-50 on amyloid-β (Aβ) oligomers in the brains of AβPP-Tg mice by immunohistochemistry. In vitro, we observed a direct effect of gx-50 on Aβ oligomers by atomic force microscopy, detected the neuroprotective effects of gx-50 by western blotting and cell apoptosis assays, and measured its effects on intracellular calcium currents by laser confocal microscopy. Experiments in vivo showed that gx-50 could penetrate the blood brain barrier and improve the cognitive abilities of mice. Moreover, gx-50 treatment decreased the accumulation of Aβ oligomers in the cerebral cortex. The results in vitro demonstrated that gx-50 could disassemble Aβ oligomers, inhibit Aβ-induced neuronal apoptosis and apoptotic gene expression, and reduce neuronal calcium toxicity. These results strongly suggest that gx-50 is a potential candidate drug for treating AD.
    Journal of Alzheimer's disease: JAD 11/2012; 34(1). DOI:10.3233/JAD-121831 · 4.15 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Vascular smooth muscle cells (SMCs) and endothelial cells (ECs) play important roles in nicotine-induced cardiovascular disease. To elucidate the mechanism underlying the abnormal SMC behavioral response to nicotine, we investigated the activation of the NF-κB signal transduction pathway and cell adhesion molecular (CAM) expression on SMCs. Also we used different cell culture manner of SMC sole and EC-SMC co-culture with a 0.4 or a 3μm membrane pore, to observe whether there is a crosstalk between EC/SMC involved in the process of NF-κB pathway activation. Nicotine-induced effects were observed in SMCs by both monoculture and co-culture with the 3μm-pore size, including the phosphorylation of IKK and IκB, the shift of transcription factor NF-κB, and the enhancement of SMC cytoskeleton protein expression and migration ability, but none were observed by co-culture with the 0.4μm-pore size. All of the actions could be distinctly blocked by α-bungarotoxin (α7 nicotinic receptor inhibitor) or PDTC (NF-κB suppressor). Flow cytometry analysis showed that the adhesion molecules ICAM-1 and LFA-1 and VCAM-1 and VLA-4 were better expressed similarly on the surface of SMCs in the monoculture and 3μm-pore size co-culture system vs. the 0.4μm's co-culture way. The results imply that nicotine induces SMC cytoskeleton protein up-expression and migration via the NF-κB signaling pathway and that EC-SMC crosstalk via CAM facilitates its response to nicotine.
    The international journal of biochemistry & cell biology 11/2012; 45(2). DOI:10.1016/j.biocel.2012.10.016 · 4.24 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Male infertility is a vexing yet common problem for men all over the world. However, its etiology remains unknown in most cases. The aim of this study was to screen and investigate the differentially expressed proteins in the sperm of infertile patients, whose sperm clinical parameters met the WHO guidelines. Using MALDI-TOF/TOF analysis, we identified 24 differentially expressed proteins from the 31 most abundant different protein spots in 2D gels of sperm samples, then verified and analyzed localization in sperm of the proteins. Following data mining analysis showed that these 24 proteins were categorized into five functional clustering groups: sexual reproduction, response to wounding, metabolic process, cell growth and/or maintenance, not clear. Additionally, 9 of the 24 differentially expressed proteins are involved in a main pathway network including TGF-β1, MYC, β-estradiol, MYCN, and TP53, which are known to be involved in cell communication, proliferation and differentiation. The observed differences in signaling and metabolic pathways between the infertile sperm and the normal fertile spermatozoa have implications in sperm motility, capacitation, acrosomal reaction and sperm-oocyte communication. These proteins are potential diagnostic markers, and the study of these proteins could help gain further insight into the pathogenic mechanisms in infertility.
    Journal of proteomics 07/2012; 75(17):5426-36. DOI:10.1016/j.jprot.2012.06.021 · 3.93 Impact Factor
  • Xiujuan Li · Yanyan Bao · Peng Fang · Yaping Chen · Zhongdong Qiao
    [Show abstract] [Hide abstract]
    ABSTRACT: To study the influence of mifepristone on the expression of cyclooxygenase 2 (COX-2) protein and COX-2 mRNA and then to evaluate the mechanism. After the establishment of 30 mice endometriosis models, the mice were randomly divided into six groups with 5 mice each group and assigned to experimental and control groups of 1-, 4- and 6-week circle according to whether mifepristone (0.13 mg d(-1)) was taken or not. Small animal optical imaging system was used to detect the fluorescent intensity of the ectopic tissue. Reverse transcript-polymerase chain reaction and western blot was used to examine COX-2 protein and COX-2 mRNA expression. ELISA was used to examine concentration of PGE(2) in serum. Mifepristone could not affect the fluorescent intensity of the ectopic endometrium after it was taken 1, 4, and 6 (P > 0.05). However, it could decrease the transcription of COX-2 mRNA in the 1 and 4 week groups (P < 0.05), while the difference in the 6 week group was not significant (P > 0.05). It could decrease the expression of COX-2 protein after it was taken 4 and 6 weeks (P < 0.05). The serous PGE(2) in the trial groups was lower than that in the control groups, but the difference was not significant (P > 0.05). This study showed that mifepristone could not affect the size of the ectopic endometrium, but it could decrease the transcription of COX-2 gene and then reduce the expression of COX-2 protein and its product PGE(2) which is an important factor which mediate pain. This maybe another mechanism that mifepristone takes effect through anti-inflammatory path.
    Archives of Gynecology 05/2012; 286(4):939-46. DOI:10.1007/s00404-012-2379-2 · 1.28 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: The role of heat shock protein 90 inhibitor geldanamycin (GA) during Leishmania donovani promastigote-to-amastigote transformation in axenic conditions was investigated. Promastigotes exhibited apoptotic morphologic changes after GA treatment at a high temperature, and the effect is in a dose- and time-dependant manner. Meanwhile, cell cycle analysis showed a significant increase at the expense of cells in the G0/G1 phase and a decrease in the S and G2/M phases after GA treatment. In addition, cellular glutathione level was reduced and reactive oxygen species content was increased afterwards. Pretreatment with antioxidants reduced the percentage of GA-induced cell apoptosis. After treatment, cultures in pH 5.5 showed a lower percentage of apoptosis than those in pH 7.4. The present study showed that GA could cause apoptosis in L. donovani but could not cause stage differentiation in high temperature and that acidic conditions were likely to be crucial for the transformation and survival of the parasite within its human host.
    Parasitology Research 09/2009; 105(6):1539-48. DOI:10.1007/s00436-009-1582-y · 2.33 Impact Factor

Publication Stats

266 Citations
89.11 Total Impact Points

Institutions

  • 2012–2015
    • Shanghai University
      Shanghai, Shanghai Shi, China
  • 2005–2014
    • Shanghai Jiao Tong University
      • • School of Life Science and Biotechnology
      • • School of Medicine
      Shanghai, Shanghai Shi, China
    • Renji Hospital
      Shanghai, Shanghai Shi, China