82nd Hospital of the Peoples Liberation Army

Huaian, China

82nd Hospital of the Peoples Liberation Army

Huaian, China

Time filter

Source Type

Jiang S.,82nd Hospital of the Peoples Liberation Army | Jiang S.,Bengbu Medical College | Zhao C.,82nd Hospital of the Peoples Liberation Army | Zhao C.,Bengbu Medical College | And 16 more authors.
International Journal of Molecular Medicine | Year: 2016

Several aberrant microRNAs (miRNAs or miRs) have been implicated in esophageal cancer (EC), which is widely prevalent in China. However, their role in EC tumorigenesis has not yet been fully elucidated. In the present study, we determined that miR1 was downregulated in esophageal squamous cell carcinoma (ESCC) tissues compared with adjacent non-neoplastic tissues using RT-qPCR, and confirmed this using an ESCC cell line. Using a nude mouse xenograft model, we confirmed that the re-expression of miR1 significantly inhibited ESCC tumor growth. A tetrazolium assay and a trypan blue exclusion assay revealed that miR1 suppressed ESCC cell proliferation and increased apoptosis, whereas the silencing of miR1 promoted cell proliferation and decreased apoptosis, suggesting that miR1 is a novel tumor suppressor. To elucidate the molecular mechanisms of action of miR1 in ESCC, we investigated putative targets using bioinformatics tools. MET, cyclin D1 and cyclin-dependent kinase 4 (CDK4), which are involved in the hepatocyte growth factor (HGF)/MET signaling pathway, were found to be targets of miR1. miR1 expression inversely correlated with MET, cyclin D1 and CDK4 expression in ESCC cells. miR1 directly targeted MET, cyclin D1 and CDK4, suppressing ESCC cell growth. The newly identified miR1/MET/cyclin D1/CDK4 axis provides new insight into the molecular mechanisms of ESCC pathogenesis and indicates a novel strategy for the diagnosis and treatment of ESCC.


Ji C.,Nanjing Medical University | Chen X.,Nanjing Medical University | Gao C.,Jinling Hospital | Jiao L.,82nd Hospital of the Peoples Liberation Army | And 5 more authors.
Journal of Bioenergetics and Biomembranes | Year: 2011

Interleukin-6 (IL-6) has emerged as an important cytokine involved in the regulation of metabolism. However, the role of IL-6 in the etiology of obesity and insulin resistance is not fully understood. Mitochondria are key organelles of energy metabolism, and there is growing evidence that mitochondrial dysfunction plays a crucial role in the pathogenesis of obesity-associated insulin resistance. In this study, we determined the direct effect of IL-6 on lipolysis in adipocytes, and the effects of IL-6 on mitochondrial function were investigated. We found that cells treated with IL-6 displayed fewer lipids and an elevated glycerol release rate. Further, IL-6 treatment led to decreased mitochondrial membrane potential, decreased cellular ATP production, and increased intracellular ROS levels. The mitochondria in IL-6-treated cells became swollen and hollow with reduced or missing cristae. However, insulin-stimulated glucose transport was unaltered. PGC-1α, NRF1, and mtTFA mRNA levels were markedly increased, and the mitochondrial contents were also increased. Our results demonstrate that IL-6 can exert a direct lipolytic effect and induce mitochondrial dysfunction. However, IL-6 did not affect insulin sensitivity in adipocytes in vitro.We deduce that in these cells, enhanced mitochondrial biogenesis might play a compensatory role in glucose transport. © Springer Science+Business Media, LLC 2011.


Qin Z.-Y.,Nanjing Medical University | Zhang M.,Nanjing Medical University | Guo X.-R.,Nanjing Medical University | Wang Y.-M.,Huaian Maternity and Child Health Hospital | And 7 more authors.
Journal of Bioenergetics and Biomembranes | Year: 2012

Overexpression of the Homo sapiens LY R motif containing 1 (LYRM1) causes mitochondrial dysfunction and induces insulin resistance in 3T3-L1 adipocytes. α-Lipoic acid (α-LA), a dithiol compound with antioxidant properties, improves glucose transport and utilization in 3T3-L1 adipocytes. The aim of this study was to investigate the direct effects of α-LA on reactive oxygen species (ROS) production and insulin sensitivity in LYRM1 overexpressing 3T3-L1 adipocytes and to explore the underlying mechanism. Pretreatment with α-LA significantly increased both basal and insulin-stimulated glucose uptake and insulin-stimulated GLUT4 translocation, while intracellular ROS levels in LYRM1 overexpressing 3T3-L1 adipocytes were decreased. These changes were accompanied by a marked upregulation in expression of insulin-stimulated tyrosine phosphorylation of IRS-1 and serine phosphorylation of Akt following treatment with α-LA. These results indicated that α-LA protects 3T3-L1 adipocytes from LYRM1-induced insulin resistance partially via its capacity to restore mitochondrial function and/or increase phosphorylation of IRS-1 and Akt. © Springer Science+Business Media, LLC 2012.


Xu G.,82nd Hospital of the Peoples Liberation Army | Ji C.,Nanjing Medical University | Song G.,Nanjing Medical University | Zhao C.,82nd Hospital of the Peoples Liberation Army | And 9 more authors.
International Journal of Obesity | Year: 2015

Background:MicroRNAs (miRNAs) have emerged as epigenetic regulators of metabolism and energy homeostasis. There is a growing body of evidence pointing to miRNAs that have important regulatory roles in insulin sensitivity.Objective:The aim of this work was to explore the expression and mechanism of action of miR-26b in obesity-related insulin resistance (IR) in adipocytes.Methods:Quantitative real-time PCR was performed to determine miR-26b expression in obese rodent models, human obesity subjects and insulin-resistant adipocytes. We analysed the roles of miR-26b overexpression and inhibition on glucose uptake in adipocytes. Western blotting was used to detect the levels of protein molecules involved in the phosphoinositide-3-kinase (PI3K) pathway. Bioinformatics and the Dual Luciferase Assay were used to identify the target gene of miR-26b. We assessed the regulatory roles of miR-26b on the phosphatase and tensin homologue (PTEN)/PI3K/AKT pathway and the relationship between miR-26b and the metabolism of human obese subjects.Results:Levels of miR-26b are reduced in visceral adipose tissue (VAT) in obese rodent models, human obesity and insulin-resistant adipocytes. MiR-26b promotes insulin-stimulated glucose uptake and increases insulin-stimulated glucose transporter type 4 translocation to the plasma membrane in human mature adipocytes. MiR-26b modulates insulin-stimulated AKT activation via inhibition of its target gene, PTEN, and significantly increases insulin sensitivity via the PTEN/PI3K/AKT pathway. The expression level of miR-26b negatively correlates with increasing body mass index and homeostasis model assessment for IR in human obese subjects.Conclusion:Decreased miR-26b expression in VAT may be involved in obesity-related IR by interrupting the PTEN/PI3K/AKT pathway. © 2015 Macmillan Publishers Limited.


Xu G.,82nd Hospital of the Peoples Liberation Army | Ji C.,82nd Hospital of the Peoples Liberation Army | Shi C.,Nanjing Medical University | Fu H.,82nd Hospital of the Peoples Liberation Army | And 6 more authors.
Molecular Biology Reports | Year: 2013

MicroRNAs (miRNAs) are short non-coding RNAs that are involved in post-transcriptional regulation of gene expression. Hsa-miR-26b is an intronic miRNA located in the intron of CTDSP1 (carboxy-terminal domain, RNA polymerase II, polypeptide A, small phosphatase 1). In the present study, the expression of hsa-miR-26b was examined during human preadipocyte differentiation. 15 days after induction of differentiation, mature human adipocytes were treated with adipokines. Hsa-miR-26b was differentially expressed during human preadipocyte differentiation. Tumor necrosis factor-α (TNF-α), leptin and resistin, but not interleukin-6, caused downregulation of hsa-miR-26b expression in adipocytes. These results suggest that the expression of hsa-miR-26b is affected by TNF-α, leptin and resistin and that hsa-miR-26b may be an important mediator in regulating the obesity-related insulin sensitivity and inflammatory responses. © 2012 Springer Science+Business Media Dordrecht.


Xu G.,82nd Hospital of The Peoples Liberation Army | Ji C.,Nanjing Medical University | Song G.,Nanjing Medical University | Shi C.,Nanjing Medical University | And 5 more authors.
Molecular Medicine Reports | Year: 2015

MicroRNAs (miRNAs) are short, 20-24 nucleotide non-coding RNAs, which are involved in multiple biological processes, including obesity. Our previous investigation revealed that miRNA (miR)-26b is differentially expressed in preadipocytes and mature adipocytes in humans. However, its role in the proliferation of human preadipocytes remains to be fully elucidated. In the present study, intracellular lipid accumulation was assessed using oil red O staining and the trigycerlide (TG) content was quantified using a TG assay kit, adipogenesis associated genes and cyclin D2 were analyzed using western blotting, and the effects of miR-26b on the proliferation of preadipocytes was investigated using Cell Counting Kit-8 assays and cell cycle analysis. Human preadipocytes overexpressing miR-26b exhibited increased TG content in the adipocytes. During differentiation, the protein expression levels of adipogenesis-associated marker genes, including peroxisome proliferator-activated receptor γ, CCAAT/enhancer-binding protein α, fatty acid-binding protein and hormone-sensitive lipase were upregulated in cells overexpressing miR-26b, compared with the negative control cells. In addition, growth of human preadipocytes overexpressing miR-26b occurred a slower rate and more remained in the G1 phase, compared with the negative control cells. In addition, miR-26b downregulated the protein expression of cyclin D2. These results demonstrated that miR-26b promoted differentiation and, at least party by targeting cyclin D2, attenuated cell proliferation via arresting the G1/S transition.


Xu G.,82nd Hospital of the Peoples Liberation Army | Xu G.,Nanjing Medical University | Shi C.,Nanjing Medical University | Ji C.,Nanjing Medical University | And 5 more authors.
Molecular Medicine Reports | Year: 2014

MicroRNAs (miRNAs) are short non-coding RNAs that are involved in numerous biological processes, including obesity and insulin resistance. miR-26b is an obesity-related intronic miRNA located in the intron of the carboxy-terminal domain, RNA polymerase II, polypeptide A, small phosphatase 1 gene. miR-26b is abundantly expressed in mice and mature human adipocytes, and is associated with the expression of adipokines. In the present study, the effects of energy-source materials and hormones associated with obesity, on miR-26b expression were investigated. It was demonstrated that free fatty acids (FFAs), glucose, glucocorticoids and growth hormone (GH) downregulate the expression of miR-26b in human adipocytes. The results indicate that the expression of miR-26b is affected by a variety of factors that are correlated with obesity and insulin sensitivity. Therefore, miR-26b may be an important mediator in the development of obesity-associated insulin resistance.


Guo Y.,Anhui Medical University | Wan S.Y.,82nd Hospital of the Peoples Liberation Army | Zhong X.,Anhui Medical University | Zhong M.K.,Anhui Medical University | Pan T.R.,Anhui Medical University
Neuroendocrinology Letters | Year: 2014

OBJECTIVE: To examine the effect of levothyroxine (L-T4), vitamin E or both on oxidative stress status and hippocampal apoptosis in a propylthiouracil (PTU)-induced hypothyroid rat model. METHODS: Sprague-Dawley rats were randomly divided into five groups: Control, PTU+PTU+L-T4+PTU+Vit E, PTU+Vit E+L-T4. In each group we assessed levels of serum triiodothyronine (T3), tetraiodothyronine (T4), thyroid stimulating hormone (TSH), hippocampus cellular apoptosis index (AI), hippocampus nicotinamide adenine denucleotide hydrogen (NADPH) oxidase and superoxide dismutase (SOD). RESULTS: 1) Compared with the control group, NADPH oxidase levels were significantly increased, and SOD levels were significantly reduced in the PTU groups (p<0.05). 2) Compared to the PTU group, SOD levels were significantly increased in the PTU+Vit E and PTU+L-T4+Vit E group (p<0.05). NADPH oxidase levels were significantly decreased in the PTU+L-T4, PTU+Vit E and PTU+ L-T4+Vit E group (p<0.05). 3) Compared with the control group, hippocampus AI increased significantly in the PTU group (p<0.05). Compared with the PTU group, hippocampus AI was significantly reduced in the PTU+L-T4 group and PTU+L-T4+Vit E group (p<0.05). 4) Hippocampus AI was positively correlated with NADPH oxidase expression levels in hippocampus tissue (r=0.644, p<0.01). CONCLUSION: Levothyroxine replacement therapy combined with vitamin E reduces hippocampus AI by improving oxidative stress. This study suggested that the mechanisms of hippocampus tissue injury in a hypothyroid rat model is related to hippocampus apoptosis from increased oxidative stress. © 2014 Neuroendocrinology Letters.


Zhang N.,82nd Hospital of the Peoples Liberation Army | Zhang N.,Bengbu Medical College | Fu H.,82nd Hospital of the Peoples Liberation Army | Fu H.,Jiangsu University | And 7 more authors.
Oncology Reports | Year: 2014

Esophageal squamous cell carcinoma (ESCC) is the predominant histologic subtype of esophageal cancer and is characterized by a high mortality rate and geographic differences in incidence. microRNAs (miRNAs) are small, non-coding RNAs that play important roles in the regulation of genes associated with cancer development and progression. In the present study, we demonstrated that microRNA-100 (miR-100) demonstrated markedly lower expression in the ESCC tissues as validated by quantitative reverse transcription-polymerase chain reaction (qRT-PCR). Furthermore, we found that the downregulation of miR-100 was significantly correlated with the status of lymph node metastasis in the 34 ESCC patients. Next, we investigated the role and mechanism of miR-100 in ESCC cells and found that miR-100 modulated the migration and invasion but not the apoptosis and proliferation of ESCC cells in vitro. We further demonstrated that miR-100 directly targeted the mTOR 3'UTR and repressed the expression of mTOR, a tumor-related gene. Similarly, miR-100 has been reported as a tumor suppressor by controlling cell migration and invasion, as it can target mTOR genes. These results provide insight into the potential mechanisms of miR-100 in the pathogenesis of ESCC.


Wang L.-L.,82nd Hospital of the Peoples Liberation Army | Xie H.,82nd Hospital of the Peoples Liberation Army | Fu H.-L.,82nd Hospital of the Peoples Liberation Army | Jiang S.,82nd Hospital of the Peoples Liberation Army | And 4 more authors.
Journal of Medical Case Reports | Year: 2013

Introduction. Malignant fibrous histiocytoma is a very common subtype of soft-tissue sarcoma in middle and late adulthood. However, malignant fibrous histiocytoma of the testis is very rare in adolescents. Case presentation. We report here the case of a 14-year-old Han Chinese boy, who presented with left scrotal mass lasting for 20 days along with distending pain for 5 days. A physical examination revealed a chicken egg-sized, firm, well-defined mass and unclear epididymis. A B-scan ultrasonography of the left scrotum displayed a 9.0×5.2×4.5cm medium- or low-echoic lobulated mass, which suggested a left testicular neoplasm. A fine needle aspiration cytology examination revealed that the cells obtained from the patient's testicular neoplasm were composed of myxoid spindle, and ovoid cells with nuclear atypia and mitotic activity, and arranged in a whirlpool or storiform pattern. Under histological examination, the tumor cells were arranged in a storiform pattern, which displayed mucoid matrix degeneration, and grew invasively. Consequently, a histopathological diagnosis suggested myxofibrosarcoma (or myxoid malignant fibrous histiocytoma). Conclusions: An ultrasonic examination combined with fine needle aspiration cytology should be helpful for the initial differential diagnosis of testicular malignant fibrous histiocytoma. However, the final confirmation relies on histopathological examination. To the best of our knowledge, this is the first reported case of malignant fibrous histiocytoma of the testis in an adolescent. © 2013 Wang et al.; licensee BioMed Central Ltd.

Loading 82nd Hospital of the Peoples Liberation Army collaborators
Loading 82nd Hospital of the Peoples Liberation Army collaborators