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Featured researches published by Ruilan Wang.


Journal of Cellular and Molecular Medicine | 2016

HIF-1α regulates EMT via the Snail and β-catenin pathways in paraquat poisoning-induced early pulmonary fibrosis.

Yong Zhu; Jiuting Tan; Hui Xie; Jinfeng Wang; Xiaoxiao Meng; Ruilan Wang

Paraquat (PQ) poisoning‐induced pulmonary fibrosis is one of the primary causes of death in patients with PQ poisoning. Hypoxia‐inducible factor‐1α (HIF‐1α) and epithelial‐mesenchymal transition (EMT) are involved in the progression of pulmonary fibrosis. Snail and β‐catenin are two other factors involved in promoting EMT. However, the relationship among HIF‐1α, Snail and β‐catenin in PQ poisoning‐induced pulmonary fibrosis is not clear. Our research aimed to determine whether the regulation of HIF‐1α in EMT occurs via the Snail and β‐catenin pathways in PQ poisoning‐induced pulmonary fibrosis. Sixty‐six Sprague–Dawley rats were randomly and evenly divided into a control group and a PQ group. The PQ group was treated with an intragastric infusion of a 20% PQ solution (50 mg/kg) for 2, 6, 12, 24, 48 and 72 hrs. A549 and RLE‐6TN cell lines were transfected with HIF‐1α siRNA for 48 hrs before being exposed to PQ. Western blotting, real‐time quantitative PCR, immunofluorescence, immunohistochemistry and other assays were used in our research. In vivo, the protein levels of HIF‐1α and α‐SMA were increased at 2 hrs and the level of ZO‐1 (Zonula Occluden‐1) was reduced at 12 hrs. In vitro, the transient transfection of HIF‐1α siRNA resulted in a decrease in the degree of EMT. The expression levels of Snail and β‐catenin were significantly reduced when HIF‐α was silenced. These data demonstrate that EMT may be involved in PQ poisoning‐induced pulmonary fibrosis and regulated by HIF‐1α via the Snail and β‐catenin pathways. Hypoxia‐inducible factor‐1α may be a therapeutic target for the treatment of PQ poisoning‐induced pulmonary fibrosis.


Experimental Biology and Medicine | 2013

Expression and significance of HIF-1α in pulmonary fibrosis induced by paraquat.

Hui Xie; Jiuting Tan; Ruilan Wang; Xiaoxiao Meng; Xue Tang; Shan Gao

It is commonly accepted that epithelial–mesenchymal transition contributes to fibrotic remodeling, but the molecular pathways involved in paraquat (PQ)-induced epithelial–mesenchymal transition remain uncharacterized. The objective of this study was to evaluate the potential involvement of HIF-1α in TGF-β1/β-Catenin and Snail pathway after PQ poisoning. In our study, 86 Spragne-Dawley rats were randomly divided into control group and PQ group, which received intragastric infusion of 20% PQ solution 50 mg/kg. Rats in the PQ group were subsequently divided into eight subgroups (10 for each subgroup) and samples were collected at different predetermined time points (2, 6, 12, 24, 48, 72, 96 h and 7 d). Fibrosis markers, including β-catenin, snail and α-SMA, were measured by western blot. The activity of HIF-1α was determined by western blot and immunofluorescence. We found that in PQ-induced pulmonary fibrosis, the level of PaO2 was significantly reduced in the 6-h subgroup, when compared to the control group (P < 0.01). Interestingly, between 6 and 72 h, there was no significant difference in PaO2. On the other hand, the level of PaCO2 started to increase from 72-h subgroup (P < 0.01). Fibrosis markers including β-catenin, snail and α-SMA, measured by western blot, were significantly increased at 2 h, while the level of p-GSK-3β was increased at 6 h. And the level of GSK-3β showed significant reduction beginning at 24 h. The activity of HIF-1α measured by western blot assays was significantly increased starting from 2 h with sustained expression. The result of Pearson coefficient analysis showed that HIF-1α was positively correlated with Snail (r = 0.935, P < 0.01) and β-catenin (r = 0.761, P < 0.05). Meanwhile, immunofluorescent analysis of HIF-1α revealed partial staining appearing from 2 h. Our data illustrated a positive correlation between Snail, β-catenin signaling and HIF-1α, suggesting a potential synergistic role of HIF-1α in PQ-induced pulmonary fibrosis, which may be independent of GSK-3β. It might also represent a potential therapeutic window for treatment of paraquat poisoning.


Journal of Cellular and Molecular Medicine | 2017

A positive feedback loop promotes HIF-1α stability through miR-210-mediated suppression of RUNX3 in paraquat-induced EMT

Yong Zhu; Jinfeng Wang; Xiaoxiao Meng; Hui Xie; Jiuting Tan; Xinkun Guo; Peng Han; Ruilan Wang

Irreversible pulmonary fibrosis induced by paraquat (PQ) poisoning is the major cause of death in patients with PQ poisoning. The epithelial–mesenchymal transition (EMT) is postulated to be one of the main mechanisms of pulmonary fibrosis. Here, we investigated the role of miR‐210 in PQ‐induced EMT and its relationship with hypoxia‐inducible factor‐1α (HIF‐1α). Western blotting, immunofluorescence, immunoprecipitation and other methods were used in this study. We found that miR‐210 expression was significantly increased after PQ poisoning, and it may be regulated by HIF‐1α. Overexpression of miR‐210 further increased the HIF‐1α protein level and promoted EMT. Moreover, miR‐210 knock‐down reduced the HIF‐1α protein level and decreased the degree of EMT. Runt‐related transcription factor‐3 (RUNX3), a direct target of miR‐210, was inhibited by miR‐210 in response to PQ poisoning. RUNX3 increased the hydroxylation ability of prolyl hydroxylase domain‐containing protein 2 (PHD2), a key enzyme that promotes HIF‐1α degradation. PHD2 immunoprecipitated with RUNX3 and its level changed similarly to that of RUNX3. The expression of the HIF‐1α protein was significantly reduced when RUNX3 was overexpressed. HIF‐1α protein levels were markedly increased when RUNX3 was silenced. Based on these results, a positive feedback loop may exist between miR‐210 and HIF‐1α. The mechanism may function through miR‐210‐mediated repression of RUNX3, which further decreases the hydroxylation activity of PHD2, enhances the stability of HIF‐1α, and promotes PQ‐induced EMT, aggravating the progression of pulmonary fibrosis. This study further elucidates the mechanism of PQ‐induced pulmonary fibrosis and may provide a new perspective for the future development of therapies.


Emerging microbes & infections | 2017

Nuclear translocation of HIF-1α induced by influenza A (H1N1) infection is critical to the production of proinflammatory cytokines

Xinkun Guo; Zhaoqin Zhu; Wanju Zhang; Xiaoxiao Meng; Yong Zhu; Peng Han; Xiaohui Zhou; Yunwen Hu; Ruilan Wang

Infection with the influenza A (H1N1) virus is a major challenge for public health because it can cause severe morbidity and even mortality in humans. The over-secretion of inflammatory cytokines (cytokine storm) is considered to be a key contributor to the severe pneumonia caused by H1N1 infection. It has been reported that hypoxia-inducible factor 1-alpha (HIF-1α) is associated with the production of proinflammatory molecules, but whether HIF-1α participates in the acute inflammatory responses against H1N1 infection is still unclear. To investigate the role of HIF-1α in H1N1 infection, the expression and nuclear translocation of HIF-1α in A549 and THP-1 cell lines infected with H1N1 virus were observed. The results showed that without altering the intracellular mRNA or protein expression of HIF-1α, H1N1 infection only induced nuclear translocation of HIF-1α under normal oxygen concentrations. The use of 2-methoxyestradiol (2ME2), a HIF-1α inhibitor that blocks HIF-1α nuclear accumulation, in H1N1-infected cells decreased the mRNA and protein expression of tumor necrosis factor-alpha (TNF-α) and interleukin (IL)-6 and increased the levels of IL-10. In contrast, H1N1-infected cells under hypoxic conditions had increased HIF-1α nuclear accumulation, increased expression of TNF-α and IL-6 and decreased levels of IL-10. In conclusion, our data implied that in vitro H1N1 infection induced nuclear translocation of HIF-1α without altering the expression of HIF-1α, which may promote the secretion of proinflammatory cytokines during H1N1 infection. Emerging Microbes & Infections (2017) 6, e39; doi:10.1038/emi.2017.21; published online 24 May 2017


World journal of emergency medicine | 2013

Effect of ulinastatin on paraquat-induced-oxidative stress in human type II alveolar epithelial cells

Xiaoxiao Meng; Ruilan Wang; Shan Gao; Hui Xie; Jiuting Tan; Yong-bin Qian

BACKGROUND: Ulinastatin (UTI) is a urinary trypsin inhibitor extracted and purified from urine of males. This study aimed to explore the effects of UTI on paraquat-induced-oxidative stress in human type II alveolar epithelial cells. METHODS: The human type II alveolar epithelial cells, A549 cells, were cultured in vitro. The A549 cells were treated with different concentrations of paraquat (200, 400, 600, 800, 1 000, 1 200 µmol/L) and ulinastatin(0, 2 000, 4 000, 6 000, 8 000 U/mL) for 24 hours, the cell viability was measured by cell counting kit-8 and the median lethal concentration was selected. In order to establish an in vitro model of paraquat intoxication and to determine the safe dose of ulinastatin, we calculated LD50 using cell counting kit-8 to determine the survival rate of the cells. A549 cells were divided into normal control group, paraquat group and paraquat+ulinastatin group. The levels of malondialdehyde (MDA) and myeloperoxidase (MPO) were detected by biochemistry colorimetry, while the level of reactive oxygen spies (ROS) was detected by DCFH-DA assay. RESULTS: The survival rate of A549 cells treated with different concentrations of paraquat decreased in a concentration-dependent manner. Whereas there was no decrease in the survival rate of cells treated with 0–4 000 U/mL ulinastatin. The levels of MDA, MPO, and ROS were significantly higher in the paraquat group than in the normal control group after 24-hour-exposure. And the survival rate of the paraquat+ulinastatin group was higher than that of the paraquat group, but lower than that of the normal control group. The levels of MDA, MPO, and ROS were lower than those of the paraquat group. CONCLUSION: Ulinastatin can alleviate the paraquat-induced A549 cell damage by reducing oxidative stress.


Life Sciences | 2018

Atorvastatin attenuates paraquat poisoning-induced epithelial-mesenchymal transition via downregulating hypoxia-inducible factor-1 alpha

Jiang Du; Yong Zhu; Xiaoxiao Meng; Hui Xie; Jinfeng Wang; Zhigang Zhou; Ruilan Wang

Aim: This study investigated the effects of atorvastatin (ATS) on the paraquat (PQ)‐induced epithelial‐mesenchymal transition (EMT) and the potential mechanism through hypoxia‐inducible factor‐1 alpha (HIF‐1&agr;). Main methods: Sprague–Dawley (SD) rats were randomly divided into a control group (n = 5), PQ group (n = 20), PQ + ATS L group (n = 20, ATS 20 mg/kg daily) and PQ + ATS H group (n = 20, ATS 40 mg/kg daily). All treated rats were given a 20% PQ solution (50 mg/kg) once by gavage and then sacrificed 12, 24, 72 and 168 h after PQ exposure. The A549 and RLE‐6TN cell lines were treated with ATS, PQ or both for 24 h. Mesenchymal (&agr;‐SMA and vimentin) and epithelial (E‐cadherin and ZO‐1) cell marker expression was tested both in vivo and in vitro. The effects of ATS on HIF‐1&agr; and &bgr;‐catenin expression were also evaluated. Key findings: ATS alleviated PQ poisoning‐induced lung injury and pulmonary fibrosis in vivo. This effect was dose‐dependent. ATS treatment attenuated the EMT by increasing the levels of the epithelial markers E‐cadherin and ZO‐1 and by decreasing the expression of the mesenchymal markers &agr;‐SMA and vimentin in both lung tissues and in vitro cell culture. In addition, ATS treatment may decrease the HIF‐1&agr; and &bgr;‐catenin levels both in vivo and in vitro. Significance: In conclusion, ATS can attenuate PQ‐induced pulmonary fibrosis. The mechanism may involve the downregulation of the HIF‐1&agr;/&bgr;‐catenin pathway and the inhibition of the PQ‐induced EMT by ATS. ATS may be considered as a therapeutic agent for PQ poisoning‐induced pulmonary fibrosis.


American Journal of Emergency Medicine | 2018

Penta-therapy for severe acute hyperlipidemic pancreatitis

Jian Lu; Yun Xie; Jiang Du; Mei Kang; Wei Jin; Yan Li; Hui Xie; Ruijie Cheng; Rui Tian; Ruilan Wang

Introduction The purpose of our study is to evaluate the efficacy of penta‐therapy for HL‐SAP in a retrospective study. Methods Retrospective study between January 2007 and December 2016 in a hospital intensive care unit. HL‐SAP patients were assigned to conventional treatment alone (the control group) or conventional treatment with the experimental protocol (the penta‐therapy group) consists of blood purification, antihyperlipidemic agents, low‐molecular weight heparin, insulin, covering the whole abdomen with Pixiao (a traditional Chinese medicine). Serum triglyceride, serum calcium, APACHE II score, SOFA score, Ranson score, and other serum biomarkers were evaluated. The hospital length of stay, local complications, systematic complications, rate of recurrence, overall mortality, and operation rate were considered clinical outcomes. Results 63 HL‐SAP patients received conventional treatment alone (the control group) and 25 patients underwent penta‐ therapy combined with conventional treatment (the penta‐therapy group). Serum amylase, serum triglyceride, white blood cell count, C‐reactive protein, and blood sugar were significantly reduced, while serum calcium was significantly increased with penta‐therapy. The changes in serum amylase, serum calcium were significantly different between the penta‐therapy and control group on 7th day after the initiation of treatment. The reduction in serum triglyceride in the penta‐therapy group on the second day and 7th day were greater than the control group. Patients in the penta‐therapy group had a significantly shorter length of hospital stay. Conclusion This study suggests that the addition of penta‐therapy to conventional treatment for HL‐SAP may be superior to conventional treatment alone for improvement of serum biomarkers and clinical outcomes.


Molecular BioSystems | 2016

Lysyl oxidase promotes epithelial-to-mesenchymal transition during paraquat-induced pulmonary fibrosis

Jinfeng Wang; Yong Zhu; Jiuting Tan; Xiaoxiao Meng; Hui Xie; Ruilan Wang


Journal of Infection | 2018

Comparison the pathogen diagnosis of severe pneumonia by using next generation sequencing and traditional detection methods, China, 2010-2018

Yun Xie; Jiang Du; Wei Jin; Xiaolei Teng; Ruijie Cheng; Peijie Huang; Hui Xie; Zhigang Zhou; Tienan Feng; Rui Tian; Ruilan Wang


/data/revues/07356757/v31i6/S0735675713001630/ | 2013

Repeated pulse intramuscular injection of pralidoxime chloride in severe acute organophosphorus pesticide poisoning

Xue Tang; Ruilan Wang; Hui Xie; Jiachang Hu; Wenbiao Zhao

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Hui Xie

Shanghai Jiao Tong University

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Xiaoxiao Meng

Shanghai Jiao Tong University

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Jiuting Tan

Shanghai Jiao Tong University

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Yong Zhu

Shanghai Jiao Tong University

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Jinfeng Wang

Shanghai Jiao Tong University

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Jiang Du

Shanghai Jiao Tong University

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Peng Han

Shanghai Jiao Tong University

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Rui Tian

Shanghai Jiao Tong University

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Ruijie Cheng

Shanghai Jiao Tong University

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Shan Gao

Shanghai Jiao Tong University

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