The Affiliated Jiangyin Hospital of Southeast University

Chengjiang, China

The Affiliated Jiangyin Hospital of Southeast University

Chengjiang, China
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Liu P.,The Affiliated Jiangyin Hospital of Southeast University | Zhou J.,Soochow University of China | Zhu H.,Nanjing Medical University | Xie L.,Jiangsu Province Hospital of Chinese Medicine | And 8 more authors.
Cytokine | Year: 2011

Vascular endothelial growth factor C (VEGF-C) is a key regulator of angiogenesis and lymphangiogenesis. VEGF-C is also implicated in the development of esophageal cancer. We investigated the mRNA levels of VEGF-C and its receptors in 38 esophageal squamous cell carcinoma specimens (ESCCs) and matched adjacent normal esophageal tissues via real-time PCR. The mRNA levels of VEGF-C, VEGFR-2 and VEGFR-3 were significantly upregulated in ESCCs versus respective side normal tissues. To explore the influence of VEGF-C on esophageal cancer progression, the expression of VEGF-C was manipulated in esophageal cancer cell lines TE-1 and Eca-109. VEGF-C transcription, translation and secretion were significantly enhanced in cells stably transfected with a VEGF-C overexpression vector or attenuated in VEGF-C shRNA-transfected cell lines. In vitro, TE-1 cells stably transfected with a VEGF-C overexpression vector exhibited an increased rate of cell proliferation, migration and focus formation, whereas knockdown of VEGF-C inhibited cell proliferation, migration and focus formation. Similar results were obtained for Eca-109 cells. VEGF-C mediated biological function through transcription of CNTN-1, which is implicated in tumor invasion and metastasis. The expression of VEGF-C was correlated with that of CNTN-1 and cell proliferation and migration induced by VEGF-C were reversed by silencing of CNTN-1. In addition, nude mice inoculated with VEGF-C shRNA-transfected cells exhibited a significantly decreased tumor size in vivo via reduced VEGFR-2 and VEGFR-3 phosphorylation and microvessel formation. VEGF-C upregulation may be involved in esophageal tumor progression. Vector-based RNA interference (RNAi) targeting VEGF-C is a potential therapeutic method for human esophageal carcinoma. © 2011 Elsevier Ltd.

Chen Z.,Nanjing Southeast University | Yin Q.,The Affiliated Jiangyin Hospital of Southeast University | Ma G.,Nanjing Southeast University | Qian Q.,Nanjing Southeast University
Cardiovascular Diabetology | Year: 2010

Background: Four single nucleotide polymorphisms (SNPs) (rs2237892, rs2237895, rs2237897, and rs2283228) in KCNQ1 are reported to be associated with type 2 diabetes mellitus (T2DM), possibly caused by a reduction in insulin secretion and higher fasting glucose, but the results are inconsistent. We investigated whether these 4 genetic markers are associated with serum lipid metabolism in a middle-aged Chinese Han population.Methods: We enrolled 398 consecutive patients, including 180 with premature coronary artery disease (CAD) (male < 55 years, female < 65 years) and 218 controls without documented CAD. All subjects were genotyped for 4 SNPs by using the ligase detection reaction method. Fasting blood sugar (FBS) and plasma concentrations of total cholesterol, triglycerides (TG), high-density lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol (LDL-C), apolipoprotein A1(apo A1), and apolipoprotein B (apo B) were determined by standard biochemical methods. Main anthropometric and metabolic characteristics are analyzed among 3 genotypes at rs2283228, rs2237895, rs2237897, or rs2237892 in KCNQ1.Results: The 3 genotypes AA, AC, and CC were present in rs2283228 and rs2237895, and the 3 genotypes CC, CT, and TT were present in rs2237897 and rs2237892. The minor genotypes CC at rs2283228 and TT at rs2237892 were associated with higher levels of TG (P = 0.007 and 0.026, respectively). Furthermore, subjects with the CC genotype at rs2283228 had lower levels of HDL-C and apo A1 than in the other 2 genotype groups (P = 0.052 and 0.055, respectively). No other associations were detected between these 4 SNPs and FBS or other lipid parameters.Conclusions: Our data suggest that rs2283228 and rs2237892 in KCNQ1 are associated with lipid metabolism in a middle-aged Chinese Han population. © 2010 Chen et al; licensee BioMed Central Ltd.

Zhou J.,Soochow University of China | Zhou J.,Nanjing Medical University | Zhou J.,The University of Oklahoma Health Sciences Center | Zhang S.,Soochow University of China | And 8 more authors.
Cancer Science | Year: 2012

The present study investigated the transcriptional regulation of low-fidelity translesion DNA synthesis (TLS) polymerases in human esophageal carcinoma. Significantly higher mRNA expression of polymerase zeta (Polξ), RAD18, polymerase iota (Polι), and polymerase kappa (Polκ) was found in esophageal carcinomas. The increased expression of Polι in tumor samples was further confirmed by immunohistochemistry. The promoter of POLI that encodes Polι was found to be hypomethylated, although the overexpression of this gene was unlikely to be associated with methylation in tumors. We further identified Sp1 and Oct-1 binding sites present in the POLI promoter. We observed that the binding affinity of Sp1 to the POLI promoter was significantly increased in cancerous tissues and that Sp1 activated POLI gene transcription in cultured cell lines. The present study demonstrates overexpression of the TLS genes in esophageal carcinoma and identifies a key role for Sp1 in upregulating POLI gene expression. © 2012 Japanese Cancer Association.

Wang W.,Soochow University of China | Luo J.,Soochow University of China | Sheng W.,Soochow University of China | Xue J.,Soochow University of China | And 6 more authors.
International Journal of Radiation Oncology Biology Physics | Year: 2016

Purpose: To investigate the molecular changes underlying the pathogenesis of radiation-induced skin fibrosis. Methods and Materials: Rat skin was irradiated to 30 or 45 Gy with an electron beam. Protein expression in fibrotic rat skin and adjacent normal tissues was quantified by label-free protein quantitation. Human skin cells HaCaT and WS-1 were treated by x-ray irradiation, and the proteasome activity was determined with a fluorescent probe. The effect of proteasome inhibitors on Transforming growth factor Beta (TGF-B) signaling was measured by Western blot and immunofluorescence. The efficacy of bortezomib in wound healing of rat skin was assessed by the skin injury scale. Results: We found that irradiation induced epidermal and dermal hyperplasia in rat and human skin. One hundred ninety-six preferentially expressed and 80 unique proteins in the irradiated fibrotic skin were identified. Through bioinformatic analysis, the ubiquitin-proteasome pathway showed a significant fold change and was investigated in greater detail. In vitro experiments demonstrated that irradiation resulted in a decline in the activity of the proteasome in human skin cells. The proteasome inhibitor bortezomib suppressed profibrotic TGF-β downstream signaling but not TGF-β secretion stimulated by irradiation in HaCaT and WS-1 cells. Moreover, bortezomib ameliorated radiation-induced skin injury and attenuated epidermal hyperplasia. Conclusion: Our findings illustrate the molecular changes during radiation-induced skin fibrosis and suggest that targeting the ubiquitin-proteasome system would be an effective countermeasure. © 2016 Elsevier Inc.

Zhang S.,Soochow University of China | Zhang S.,Jiangsu University of Science and Technology | Zhang S.,The University of Oklahoma Health Sciences Center | Song C.,Nanjing Medical University | And 10 more authors.
Radiation Oncology | Year: 2012

Objective: Radiation-induced skin injury remains a serious concern for radiation therapy. Heme oxygenase-1 (HO-1), the rate-limiting enzyme in heme catabolism, has been reported to have potential antioxidant and anti-apoptotic properties. However, the role of HO-1 in radiation-induced skin damage remains unclear. This study aims to elucidate the effects of HO-1 on radiation-induced skin injury in rats.Methods: A control adenovirus (Ad-EGFP) and a recombinant adenovirus (Ad-HO1-EGFP) were constructed. Rats were irradiated to the buttock skin with a single dose of 45 Gy followed by a subcutaneous injection of PBS, 5 × 10 9genomic copies of Ad-EGFP or Ad-HO1-EGFP (n = 8). After treatment, the skin MDA concentration, SOD activity and apoptosis were measured. The expression of antioxidant and pro-apoptotic genes was determined by RT-PCR and real-time PCR. Skin reactions were measured at regular intervals using the semi-quantitative skin injury score.Results: Subcutaneous injection of Ad-HO1-EGFP infected both epidermal and dermal cells and could spread to the surrounding regions. Radiation exposure upregulated the transcription of the antioxidant enzyme genes, including SOD-1, GPx2 and endogenous HO-1. HO-1 overexpression decreased lipid peroxidation and inhibited the induction of ROS scavenging proteins. Moreover, HO-1 exerted an anti-apoptotic effect by suppressing FAS and FASL expression. Subcutaneous injection of Ad-HO1-EGFP demonstrated significant improvement in radiation-induced skin injury.Conclusions: The present study provides evidences for the protective role of HO-1 in alleviating radiation-induced skin damage in rats, which is helpful for the development of therapy for radiation-induced skin injury. © 2012 Zhang et al; licensee BioMed Central Ltd.

Huan J.,Soochow University of China | Gao Y.,The Affiliated Jiangyin Hospital of Southeast University | Xu J.,Soochow University of China | Sheng W.,Soochow University of China | And 6 more authors.
International Journal of Clinical and Experimental Pathology | Year: 2015

Objective: Esophageal squamous cell carcinoma (ESCC) is one of the leading causes of cancer deaths worldwide. CD9 has been reported to play a critical role in cell motility, growth and metastasis of multiple cancers. The present study investigated the clinicopathological features of CD9, and its biological characteristics in ESCC. Methods: Fifteen normal esophageal tissue specimens, fifty-three ESCC adjacent tissues and one hundred and four ESCC tissues were included in this study. Using immunohistochemistry (IHC), the expression levels of CD9 were evaluated among different samples. And its clinicopathological parameters and its prognostic factors were analyzed. Western blotting was used to measure CD9 expression and colony formation was performed to determine the effect of CD9 on cell growth in ESCC TE-1 cells. Results: Compared with normal esophageal tissues and tumor adjacent tissues, CD9 expression level is significantly higher in ESCC tissues. CD9 expression correlated with tumor stage (P = 0.022) and lymph node metastasis (P = 0.019) in ESCC patients. Furthermore, the small interfering RNA-mediated silencing of CD9 expression in TE-1 cells resulted in increased proliferation as evidenced by increased colony number and colony size. Conclusion: CD9 expression is upregulated in ESCC tissues and its expression is correlated with tumor stage and lymph node metastasis in ESCC patients. CD9 suppresses the proliferation of TE-1 cells. CD9 may present a potential in tumor progression in ESCC.

PubMed | Nanjing Medical University and The Affiliated Jiangyin Hospital of Southeast University
Type: Journal Article | Journal: Acta pharmacologica Sinica | Year: 2014

To investigate the effects of pyrroloquinoline quinone (PQQ), an oxidoreductase cofactor, on high glucose-induced mouse endothelial cell damage in vitro.Mouse brain microvascular endothelial bEND.3 cells were exposed to different glucose concentrations (5.56, 25 and 40 mmol/L) for 24 or 48 h. The cell viability was examined using MTT assay. Flow cytometry was used to analyze the apoptosis and ROS levels in the cells. MitoTracker Green staining was used to examine the mitochondria numbers in the cells. Western blot analysis was used to analyze the expression of HIF-1 and the proteins in JNK pathway.Treatment of bEND.3 cells with high glucose significantly decreased the cell viability, while addition of PQQ (1 and 10 mol/L) reversed the high glucose-induced cell damage in a concentration-dependent manner. Furthermore, PQQ (100 mol/L) significantly suppressed the high glucose-induced apoptosis and ROS production in the cells. PQQ significantly reversed the high glucose-induced reduction in both the mitochondrial membrane potential and mitochondria number in the cells. The high glucose treatment significantly increased the expression of HIF-1 and JNK phosphorylation in the cells, and addition of PQQ led to a further increase of HIF-1 level and a decrease of JNK phosphorylation. Addition of JNK inhibitor SP600125 (10 mol/L) also significantly suppressed high glucose-induced apoptosis and JNK phosphorylation in bEND.3 cells.PQQ protects mouse brain endothelial cells from high glucose damage in vitro by suppressing intracellular ROS and apoptosis via inhibiting JNK signaling pathway.

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