Min Wang

Tongji Medical University, Wu-han-shih, Hubei, China

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Publications (175)322.24 Total impact

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    ABSTRACT: The Hippo signaling pathway plays a crucial role in regulating tissue homeostasis, organ size, tumorigenesis and cancer chemoresistance when deregulated. Physiologically, the Hippo core kinase cassette that consists of mamma-lian STE20-like protein kinase 1/2 (MST1/2), and large tumour suppressor 1/2 (LATS1/2), together with the adaptor proteins Salvador homologue 1 (SAV1) and MOB kinase activator 1 (MOB1), tightly restricts the activities of homologous oncoproteins Yes-associated protein (YAP) and transcriptional co-activator with PDZ-binding motif (TAZ) to low levels. However, how the Hippo kinase cassette core components are simultaneously inhibited, to exhibit constitutively inactivated Hippo signaling and activated YAP/TAZ in cancer remains puzzling. Herein, we reported that miR-181c directly repressed MST1, LATS2, MOB1 and SAV1 expression in human pancreatic cancer cells. Overexpression of miR-181c induced hyperactivation of the YAP/TAZ and enhanced expression of the Hippo signaling downstream genes CTGF, BIRC5 and BLC2L1, leading to pancreatic cancer cell survival and chemoresistance in vitro and in vivo. Importantly, high miR-181c levels were significantly correlated with Hippo signaling inactivation in pancreatic cancer samples, and predicted a poor patient overall survival. These findings provide a novel mechanism for Hippo signaling inactivation in cancer, indicating not only a potentially pivotal role for miR-181c in the progression of pancreatic cancer, but also may represent a new therapeutic target and prognostic marker.
    Oncotarget 11/2015; DOI:10.18632/oncotarget.6298 · 6.36 Impact Factor
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    ABSTRACT: Purpose: Retinal nerve fiber layer (RNFL) will show retrograde degeneration following damage to the optic nerve or the optic tract in patients with pituitary adenoma. RNFL changes after surgery have not been studied thoroughly in patients with the transsphenoidal surgery and patients with the transcranial surgery. Methods: Thirty-seven patients with pituitary adenoma were recruited from Huashan hospital between September 2010 and July 2014. Patients were divided into two groups: the transsphenoidal group and the transcranial group. Before surgery, 3 and 9 months after surgery, follow-up optic coherence tomography were conducted. Results: Twenty-one patients underwent transsphenoidal surgery and 16 patients underwent transcranial surgery. No obvious difference were observed between these two groups before surgery. The mean RNFL thickness did not change significantly in patients who underwent transsphenoidal surgery: 91.1 before surgery, 92.7 at 3 months after surgery (p = 0.392) and 92.8 at 9 months after surgery (p = 0.395). The mean RNFL thickness decreased in patients who underwent transcranial surgery: 93.6 before surgery, 86.1 at 3 months after surgery (p = 0.000) and 88.1 at 9 months after surgery (p = 0.005). Conclusions: In the short time follow-up, there was no change of RNFL thickness in pituitary adenoma patients underwent transsphenoidal surgery, but a decrease in patients underwent transcranial surgery.
    Pituitary 10/2015; DOI:10.1007/s11102-015-0689-7 · 3.20 Impact Factor
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    ABSTRACT: Key messages: Overactivation of RAS plays a crucial role in the development of the DN. Our aim was to verify the effectiveness of ATRQβ-001 vaccine in STZ-induced DN. The ATRQβ-001 modulated two RAS axes and inhibited TGF-β1/Smad3 signal pathway. The vaccine therapy may provide a novel, safe, and promising method to treat DN.
    Journal of Molecular Medicine 09/2015; DOI:10.1007/s00109-015-1343-6 · 5.11 Impact Factor
  • Chao Yu · Min Wang · Meiyuan Chen · Yang Huang · Jianxin Jiang ·
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    ABSTRACT: The present study investigated the role of microRNA (miR)‑138‑5p in regulating carcinoma migration and sensitivity to chemotherapy in pancreatic cancer. Reverse transcription‑quantitative polymerase chain reaction (RT‑qPCR) was used to assess the expression levels of miR‑138‑5p in pancreatic cancer cell lines and primary carcinoma tissues from human patients. A lentiviral vector, containing miR‑138‑5p mimics (lv‑miR‑138‑m) or miR‑138‑5p inhibitor (lv‑miR‑138‑i), was used to either upregulate or downregulate the expression levels of miR‑138‑5p in PANC‑1 cells, respectively. The effects of miR‑138‑3p regulation on pancreatic cancer cell migration and sensitivity to chemotherapy were examined. The predicted targeting of miR‑138‑5p on vimentin (VIM) was assessed by western blotting in PANC‑1 cells. VIM was subsequently downregulated using small interfering (si)RNA to determine its effect on miR‑138‑5p‑modulated pancreatic cancer cell development. The expression levels of miR‑138‑5p were downregulated in pancreatic cancer cell lines and primary carcinoma tissues. In PANC‑1 cells, lentivirus-mediated upregulation of miR‑138‑5p inhibited cancer cell migration and increased cell chemosensitivity to 5‑fluorouracil (5‑FU). By contrast, downregulation of miR‑138‑5p promoted cancer cell migration and decreased cell chemosensitivity to 5‑FU. A luciferase assay revealed that VIM was a direct target of miR‑138‑5p. Western blotting demonstrated that VIM was downregulated upon the upregulation of miR‑138‑5p in PANC‑1 cells. siRNA‑mediated downregulation of VIM inhibited pancreatic cancer cell migration in the control and miR‑138‑5p downregulated PANC‑1 cells. The present study demonstrated that miR‑138‑5p is important in regulating pancreatic cancer development, possibly through targeting VIM.
    Molecular Medicine Reports 07/2015; 12(4). DOI:10.3892/mmr.2015.4031 · 1.55 Impact Factor
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    ABSTRACT: The conserved polarity complex, which comprises partitioning-defective proteins Par3, Par6, and the atypical protein kinase C, affects various cell-polarization events, including assembly of tight junctions. Control of tight junction assembly is closely related to invasion and migration potential. However, as the importance of conserved polarity complexes in regulating pancreatic cancer invasion and metastasis is unclear, we investigated their role and mechanism in pancreatic cancers. We first detect that the key protein of the conserved polarity complex finds that only Par3 is down-regulated in pancreatic cancer tissues while Par6 and aPKC show no difference. What is more, Par3 tissues level was significantly and positively associated with patient overall survival. Knocking-down Par3 promotes pancreatic cancer cells invasion and migration. And Par3 requires interaction with Tiam1 to affect tight junction assembly, and then affect invasion and migration of pancreatic cancer cells. Then, we find that tight junction marker protein ZO-1 and claudin-1 are down-regulated in pancreatic cancer tissues. And the relationship of the expression of Par3 and ZO-1 in pancreatic cancer tissue is linear correlation. We establish liver metastasis model of human pancreatic cancer cells in Balb/c nude mice and find that knocking down Par3 promotes invasion and metastasis and disturbs tight junction assembly in vivo. Taken together, these results suggest that the Par3 regulates invasion and metastasis in pancreatic cancers by controlling tight junction assembly.
    Clinical and Experimental Medicine 06/2015; DOI:10.1007/s10238-015-0365-2 · 2.96 Impact Factor
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    ABSTRACT: Purpose: The prognosis of pancreatic cancer ranks among the worst of all cancer types, which is primarily due to the fact that during the past decades little progress has been made in its diagnosis and treatment. Here, we set out to investigate the role of microRNA 138 (miR-138-5p) in the regulation of pancreatic cancer cell growth and to assess its role as putative therapeutic target. Methods: qRT-PCR was used to examine the expression of miR-138-5p in 8 pancreatic cancer cell lines and 18 primary human pancreatic cancer samples. A lentivirual vector containing miR-138-5p mimics (lv-miR-138-5p) was used to exogenously over-express miR-138-5p in the pancreatic cancer cells lines Capan-2 and PANC-1. The effect of this over-expression on cell proliferation was examined using an in vitro propidium iodide fluorescence assay. Capan-2 cells exogenously over-expressing miR-138-5p were transplanted into nude mice to examine its in vivo effect on tumor growth. A predicted target of miR-138-5p (FOXC1) was first validated using a luciferase assay and, subsequently, down-regulated by siRNA to assess its effect on pancreatic cancer cell growth. Results: We found that miR-138-5p was markedly down-regulated in both pancreatic cancer cell lines and primary human pancreatic cancer samples, compared to a human pancreas ductal epithelial (HPDE) cell line and normal pancreatic tissues, respectively (P < 0.05). In addition, we found that in the pancreatic cancer cells lines Capan-2 and PANC-1 lentiviral transfection of miR-138-5p mimicked up-regulation of the endogenous expression of miR-138-5p and, concomitantly, inhibited cancer cell proliferation (P < 0.05). The exogenous over-expression of miR-138-5p also led to a significant inhibition of tumor formation in vivo. Using a luciferase assay, we found that miR-138-5p directly targets FOXC1. In conformity with this notion, we found that FOXC1 was down-regulated upon miR-138-5p over-expression in pancreatic cancer cells. Finally, we found that silencing of FOXC1 by siRNA had an inhibitory effect on pancreatic cancer cell growth. Conclusions: Our data indicate that miR-138-5p may play an important role in regulating pancreatic cancer cell growth, possibly through targeting FOXC1. Over-expression of miR-138-5p may serve as a novel approach for the treatment of patients with pancreatic cancer.
    Cellular Oncology 02/2015; 38(3). DOI:10.1007/s13402-014-0200-x · 3.03 Impact Factor
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    ABSTRACT: We intended to investigate the role of microRNA 137 (miR-137) in regulating pancreatic cancer cells' growth in vitro and tumor development in vivo. QTR-PCR was used to examine the expression of miR-137 in pancreatic cancer cell lines and tumor cells from human patients. Lentivirual vector containing miR-137 mimic was used to overexpress miR-137 in PANC-1 and MIA PaCa-2 cells. The effects of overexpressing miR-137 on pancreatic cancer cell invasion and chemo-sensitivity to 5-fluorouracil (5-FU) were examined by cell migration and survival essays in vitro. The molecular target of miR-137, pleiotropic growth factor (PTN), was down-regulated by siRNA to examine its effects on cancer cell invasion. MIA PaCa-2 cells with endogenously overexpressed miR-137 were transplanted into null mice to examine tumor growth in vivo. We found miR-137 was markedly underexpressed in both pancreatic cancer cell lines and tumor cells from patients. In cancer cells, transfection of lentivirus containing miR-137 mimic was able to markedly upregulate endogenous expression of miR-137, inhibited cancer cell invasion and increased sensitivities to chemotherapy reagent 5-FU. PTN was significantly down-regulated by overexpressing miR-137 in pancreatic cancer cells, and knocking down PTN was effective to rescue the reduced cancer cell invasion ability caused by miR-137 overexpression. More importantly, overexpressing miR-137 led to significant inhibition on tumor formation, including reductions in tumor weight and tumor size in vivo. Our study demonstrated that miR-137 played an important role in pancreatic cancer development. It may become a new therapeutic target for gene therapy in patients suffered from pancreatic cancer.
    International journal of clinical and experimental pathology 12/2014; 7(11):7442-50. · 1.89 Impact Factor
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    ABSTRACT: Postoperative pancreatic fistula remains the most common complication of pancreaticoduodenectomy (PD) and is potentially lethal. It contributes significantly to prolonged hospitalization and mortality. In this study, we introduced a new technical approach, a modified Roux-en-Y reconstruction and evaluated its safety and feasibility. We retrospectively reviewed the patients who had undergone PD with the modified Roux-en-Y reconstructive technique for periampullary malignancies from January 2011 to June 2012. The data on complications, hospital stay and outcomes after the modified Roux-en-Y reconstruction were analyzed. The reconstruction was performed in 171 patients, of whom 92 received pancreaticogastrostomy and 79 received pancreaticojejunostomy. The median duration of surgery was 4.0 hours (range 3.1-6.9) in all patients, and the median blood loss was 530 mL (range 200-2000). Sixty-nine patients were subjected to transfusions, with a median transfusion volume of 430 mL (range 200-1400). The median hospital stay of the patients was 14 days (range 11-38). Their operative mortality was zero and overall morbidity was 18.1% (31 patients). Only four patients (2.3%) developed pancreatic fistulas (grade A fistulas in two patients and grade B in two patients); no patients developed grade C fistula. None of the patients developed bile reflux gastritis. The modified Roux-en-Y reconstruction, which isolates biliary anastomosis from pancreatic, gastric or jejunal anastomosis, is a safe, reliable, and favorable technique. But it needs further investigation in randomized controlled trials.
    Hepatobiliary & pancreatic diseases international: HBPD INT 12/2014; 13(6):649-53. DOI:10.1016/S1499-3872(14)60047-3 · 1.17 Impact Factor
  • Ye-Chen Feng · Min Wang · Feng Zhu · Ren-Yi Qin ·
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    ABSTRACT: Acute pancreatitis (AP) is an inflammatory disease of the pancreas which involves the pancreas and surrounding tissue, and systemic inflammation with a characteristic systemic increase of vascular permeability and increased risk of multiple organ dysfunction. Currently, the pathogenesis of AP is fuzzy, and the diagnosis and treatment need to be standardized. Nevertheless, increased knowledge of AP may achieve more thorough understanding of the pathogenesis. The use of further advanced diagnostic tools and superior treatment, potentially will help clinicians to manage AP at an appropriate stage. However, in view of the multi factorial disease and the complex clinical manifestations, the management of patients with AP is also remaining areas for improvement.
    World Journal of Gastroenterology 11/2014; 20(43):16138-16145. DOI:10.3748/wjg.v20.i43.16138 · 2.37 Impact Factor
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    ABSTRACT: Application of oxaliplatin for the treatment of pancreatic cancer (PC) is restricted owing to its toxic side effects and drug resistance. We investigated how withaferin A (WA), a bioactive component isolated from the medicinal plant Withania somnifera, acts synergistically with oxaliplatin on human PC in vitro and in vivo. We found that WA enhanced oxaliplatin-induced growth suppression and apoptosis in PC cells dramatically through a mechanism involving mitochondrial dysfunction and inactivation of the PI3K/AKT pathway. Combination treatment resulted in significant accumulation of intracellular reactive oxygen species (ROS). Pretreatment of cells with the ROS scavenger N-acetylcysteine completely blocked the apoptosis induced by combination treatment, and recovered expression of AKT inactivation, which revealed the important role of ROS in apoptosis and AKT regulation. In vivo, combination therapy showed the strongest anti-tumor effects compared with single agents, without obvious additional toxicity. These results support the notion that combination treatment with oxaliplatin and WA could facilitate development of an effective strategy for PC treatment. Copyright © 2014. Published by Elsevier Ireland Ltd.
    Cancer Letters 11/2014; 357(1). DOI:10.1016/j.canlet.2014.11.026 · 5.62 Impact Factor
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    ABSTRACT: Background: There have been no studies investigating the correlation between structural [thickness of the retinal nerve fiber layer (RNFL) as determined by optical coherence tomography (OCT)] and functional [Humphrey visual field (HVF) or visual evoked potential (VEP) amplitude] measures of optic nerve integrity in patients with pituitary adenomas (PA). Methods: Patients with PAs were recruited between September 2010 and September 2013. OCT, standard automated perimetry (SAP), and multifical VEP (mfVEP) were performed. Agreement between OCT, SAP, and mfVEP values in classifying eyes/quadrants was determined using AC1 statistics. Pearson's correlation was used to examine relationships between structural and functional data. Results: In total, 88.7 % of the eyes tested showed abnormal SAP findings and 93.7 % showed abnormal mfVEP findings. Only 14.8 % of the eyes showed abnormal OCT findings. The agreement between SAP and mfVEP findings was 88.9 % (AC1 = 0.87). The agreement between OCT and mfVEP findings was 24.2 % (AC1 = -0.52), and that between OCT and SAP findings was 21.5 % (AC1 = -0.56). The correlation values between RNFL thickness and the functional measurements were -0.601 for the mfVEP score (P = 0.000) and -0.441 for the SAP score (P = 0.000). The correlation between the mfVEP and SAP scores was -0.617 (P = 0.000). Conclusions: mfVEP, SAP, and OCT provided complementary information for detecting visual pathway abnormalities in patients with PAs. Good agreement was demonstrated between SAP and mfVEP and quantitative analysis of structure-function measurements revealed a moderate correlation.
    Pituitary 10/2014; 18(5). DOI:10.1007/s11102-014-0613-6 · 3.20 Impact Factor
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    ABSTRACT: We intended to investigate the role of microRNA 100 (miR-100) in regulating pancreatic cancer cells' growth in vitro and tumor development in vivo. QTR-PCR was used to examine the expression of miR-100 in pancreatic cancer cell lines and tumor cells from human patients. Lentivirual vector containing miR-100 mimics (lv-miR-100) was used to overexpress miR-100 in MIA PaCa-2 and FCPAC-1 cells. The effects of overexpressing miR-100 on pancreatic cancer cell proliferation and chemosensitivity to cisplatin were examined by cell proliferation essay in vitro. MIA PaCa-2 cells with endogenously overexpressed miR-100 were transplanted into null mice to examine tumor growth in vivo. The predicted target of miR-100, fibroblast growth factor receptor 3 (FGFR3), was downregulated by siRNA to examine its effect on pancreatic cancer cells. We found miR-100 was markedly underexpressed in both pancreatic cancer cell lines and tumor cells from patients. In cancer cells, transfection of lv-miR-100 was able to upregulate endogenous expression of miR-100, inhibited cancer cell proliferation, and increased sensitivities to cisplatin. Overexpressing miR-100 led to significant inhibition on tumor formation in vivo. Luciferase essay showed FGFR3 was direct target of miR-100. FGFR3 was significantly downregulated by overexpressing miR-100 in pancreatic cancer cells and knocking down FGFR3 by siRNA exerted similar effect as miR-100. Our study demonstrated that miR-100 played an important role in pancreatic cancer development, possibly through targeting FGFR3. It may become a new therapeutic target for gene therapy in patients suffered from pancreatic cancer.
    Tumor Biology 10/2014; 35(12). DOI:10.1007/s13277-014-2271-8 · 3.61 Impact Factor
  • Min Wang · Qunwei Tang · Peipei Xu · Benlin He · Lin Lin · Haiyan Chen ·
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    ABSTRACT: In order to enhance the charge-transfer ability, positively charged polyaniline-graphene complexes are synthesized by a reflux method and assembled into multilayers with negatively charged graphene oxide. The counter electrodes from polyaniline-graphene/graphene oxide (PANi-G/GO)n (n represents the bilayer number) multilayers show superior electrocatalytic activity and electrical conductivity because of enormous interface. An impressive power conversion efficiency of 7.88% is recorded from the DSSC employing PANi-G/GO multilayer counter electrode. The multilayer counter electrodes and the resultant DSSCs are thoroughly assessed by electrochemical characterizations. The results are far from optimal but the preliminary photovoltaic performances make the strategy promising in efficient DSSC applications.
    Electrochimica Acta 08/2014; 137:175–182. DOI:10.1016/j.electacta.2014.05.142 · 4.50 Impact Factor

  • Journal of the American College of Surgeons 08/2014; 219(2). DOI:10.1016/j.jamcollsurg.2014.01.066 · 5.12 Impact Factor
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    ABSTRACT: This study aimed to investigate the role in metastasis and prognostic value of KAP-1 in pancreatic cancer (PC). The expression of KAP-1 was analyzed by quantitative real-time polymerase chain reaction, Western blotting, and immunohistochemical staining in 91 human PC tissue samples. Capan-2 cells were transfected with a lentiviral vector expressing KAP-1 (Capan-2/KAP-1) or the empty vector (Capan-2/vector); cell migration and invasion were assayed in vitro using Transwell migration and wound-healing assays, and in vivo using a xenograft model in nude mice. KAP-1 was found to be overexpressed in human PC, and the expression of KAP-1 correlated with clinical stage. Overexpression of KAP-1 increased the invasion and migration of Capan-2 cells in vitro. Furthermore, overexpression of KAP-1 promoted the growth and metastatic ability of PC cells in a xenograft model in nude mice. Moreover, overexpression of KAP-1 induced the epithelial-mesenchymal transition (EMT) in PC cells both in vitro and in vivo, as indicated by increased expression of mesenchymal markers such as vimentin and decreased expression of E-cadherin. This study indicates that KAP-1 may promote metastasis in PC by regulating the EMT and suggests that KAP-1 may have potential as a predictor of metastasis in patients with pancreatic cancer.
    Medical Oncology 07/2014; 31(7):25. DOI:10.1007/s12032-014-0025-5 · 2.63 Impact Factor
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    ABSTRACT: With an aim of significantly enhancing charge-transfer ability of counter electrodes and therefore photovoltaic performances of dye-sensitized solar cells (DSSCs), here we pioneerly report the complexation of polyaniline (PANi) and graphene as well as their employment as counter electrodes (CEs) in efficient DSSCs. Owing to the covalent bond between PANi (N atoms) and graphene (C atoms), charge transfer kinetics is dramatically elevated, which can be confirmed by the enhancement on electrocatalytic activity toward triiodides and a decrease in charge-transfer resistance. A power conversion efficiency of 7.70% is determined from DSSC using PANi−8 wt‰ graphene complex CE in comparison with 6.40% from pure PANi CE-based DSSC. The high conversion efficiency, facile charge-transfer in combination with simple preparation, relatively low cost, and scalability demonstrates the potential use of PANi−graphene complexes in robust DSSCs.
    Journal of Power Sources 06/2014; 256:8–13. DOI:10.1016/j.jpowsour.2014.01.053 · 6.22 Impact Factor
  • Min Wang · Qunwei Tang · Haiyan Chen · Benlin He ·
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    ABSTRACT: Layer-by-layer self-assembly is a versatile technique for the construction of well-defined nanoarchitectures with outstanding electrical and photoelectric performances. The revelation of a potential charge-transfer mechanism of extraordinary electrical and photoelectric behaviors is profound in the design of modern electrical and photoelectrical devices. With the aim of revealing the potential charge-transfer mechanism in conducting multilayer films, in this study, we fabricated [poly(styrene sulfonate)/polyaniline]n [(PSS/PANi)n] multilayers with peculiar electrical and photoelectrical features. The fantastic increments in sheet conductivity and photoelectric response were believed to be the percolation reflection of accumulative electrons tunneled across the insulating PSS from the bottom to the top of the conjugated structure of PANi. These profound phenomena, along with simple fabrication and a well-defined architecture, promise that the conducting multilayers will be good candidates for electronic and optoelectronic nanodevices. © 2013 Wiley Periodicals, Inc. J. Appl. Polym. Sci. 2014, 131, 40258.
    Journal of Applied Polymer Science 05/2014; 131(10). DOI:10.1002/app.40258 · 1.77 Impact Factor
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    ABSTRACT: With an aim of accelerating the charge transfer between polyaniline (PANi) and graphene, polyaniline-graphene (PANi-graphene) complexes are synthesized by a reflux technique and employed as counter electrodes (CEs) for dye-sensitized solar cells (DSSCs). Owing to the easy charge-transfer between PANi (N atoms) and graphene (C atoms) by a covalent bond, electrical conduction and electrocatalysis of PANi-graphene complex CEs, and therefore power conversion efficiency of their DSSCs have been elevated in comparison with that of PANi-only CE. The resultant PANi-graphene complex CEs are characterized by spectral analysis, morphology observation, and electrochemical tests. The DSSC employing PANi-8 wt‰ graphene complex CE gives an impressive power conversion efficiency of 7.78%, which is higher than 6.24% from PANi-only and 6.52% from Pt-only CE based DSSCs.
    ACS Applied Materials & Interfaces 05/2014; 6(11). DOI:10.1021/am500981w · 6.72 Impact Factor
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    ABSTRACT: EphB2 is an important member of the receptor tyrosine kinases. Recently, EphB2 was shown to facilitate T-cell migration and monocyte activation. However, the effects of EphB2 on B cells remain unknown. In this study, the expression of EphB2 on B cells was tested by Western blot, and the roles of EphB2 in B-cell proliferation, cytokine secretion, and immunoglobulin (Ig) production were evaluated using EphB2 siRNA interference in human B cells from healthy volunteers. Our study revealed that EphB2 was distributed on naive B cells and was up-regulated on activated B cells. Moreover, B-cell proliferation (decreased by 22%, P<0.05), TNF-α secretion (decreased by 40%, P<0.01) and IgG production (decreased by 26%, P < 0.05) were depressed concordantly with the down-regulated EphB2 expression. Subsequently, we screened microRNAs that could regulate EphB2 expression in B cells, and discovered that miR-185 directly targeted to EphB2 mRNA and suppressed its expression. Furthermore, miR-185 overexpression inhibited B-cell activation, and the inhibitor of miR-185 enhanced B-cell activation. Moreover, abatement of EphB2 through miR-185 mimics or EphB2 siRNA attenuated the activation of Src-p65 and Notch1 signaling pathways in human B cells. Our study first suggested that EphB2 was involved in human naive B cell activation through Src-p65 and Notch1 signaling pathways and could be regulated by miR-185.-Yu, M., Liang, W., Wen, S., Zhao, T., Zhu, M.-X., Li, H.-H., Long, Q., Wang, M., Cheng, X., Liao, Y.-H., Yuan, J. EphB2 contributes to human naive B-cell activation and is regulated by miR-185.
    The FASEB Journal 05/2014; 28(8). DOI:10.1096/fj.13-247759 · 5.04 Impact Factor
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    ABSTRACT: Background & objectives: Angiotensin II receptor type 1 (AT1) is known to be involved in the pathogenesis of hypertension. this study was undertaken to explore the effect of active immunization against AT1 receptor on blood pressure and small artery remodelling in spontaneously hypertensive rat (SHR). Methods: Male SHR and Wistar rats aged two months were actively immunized with different peptides (ATR12185, ATR10014 and ATR12181) corresponding to particular sequences of rat AT1 receptor, while another SHR group was given losartan (10 mg/kg/day) orally once a day. Anti-AT1 receptor antibodies were detected by ELISA and blood pressure was measured. The effect of the antibodies on the artery and vascular smooth muscle cells (VSMCs) proliferation was studied. Results: All immunized animals produced antibodies against the particular peptides. The systolic blood pressure was decreased in the SHR immunized with peptide-ATR12181 compared with the control. However, no changes were observed in the SHR immunized with other two peptides. The Wistar rats immunized with the three peptides did not show any changes in blood pressure. The media/lumen area ratio of the mesenteric artery was reduced in SHR immunized with ATR12181 and similar to that of the SHR treated with losartan. The antibody from SHR immunized with ATR12181 had no effect on the proliferation of VSMC. But it could inhibit the proliferation caused by angiotensin II and its effect at the titre of 1:40 was similar to that of 1µmol/l losartan. Interpretation & conclusions: Our findings demonstrated that the antibody from SHR immunized with ATR12181 had the effect of reducing blood pressure and target organ protection similar to losartan. Active immunization against AT1 receptor may be a promising strategy in future for the treatment of hypertension.
    The Indian Journal of Medical Research 04/2014; 139(4):619-24. · 1.40 Impact Factor

Publication Stats

1k Citations
322.24 Total Impact Points


  • 2014-2015
    • Tongji Medical University
      Wu-han-shih, Hubei, China
    • Fudan University
      • Department of Ophthalmology
      Shanghai, Shanghai Shi, China
  • 2008-2014
    • Ocean University of China
      • Department of Materials Science and Engineering
      Tsingtao, Shandong Sheng, China
  • 2007-2014
    • Tongji Hospital
      Wu-han-shih, Hubei, China
  • 1970-2014
    • Huazhong University of Science and Technology
      • • Department of Cardiology
      • • Department of Biliary-Pancreatic Surgery
      • • Department of Control Science and Engineering
      • • Department of Dermatology
      Wu-han-shih, Hubei, China
  • 2006-2013
    • Wuhan Union Hospital
      Wu-han-shih, Hubei, China