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Hai B.,Huazhong University of Science and Technology | Yang Y.,Center for Molecular Physiology Research | Xiao Y.,Huazhong University of Science and Technology | Li B.,Huazhong University of Science and Technology | Chen C.,Huazhong University of Science and Technology
Journal of the Canadian Urological Association | Year: 2012

Objectives: The objective of this study is to evaluate the diagnosis and prognosis of malignant mesothelioma of the tunica vaginalis testis through an additional 6 patients with urogenital mesothe-lioma. Methods: Six patients with urogenital mesothelioma who under-went adequate surgical procedures and histopathologic analysis from 1990 to 2009 were identified and retrospectively reviewed. Results: Six patients between the ages of 26 and 78 years with urogenital mesothelioma, 5 of which originated in the scrotum and 1 in the spermatic cord. Histopathologic analysis showed that CK5/6 and calretinin were positive in all cases, 5 cases were positive for vimentin, and 1 case showed focal weak positive reaction with MOC3, but none of the cases stained for CEA or CD15. The overall recurrence rate of urogenital mesothelioma after surgery was 5/6, including local recurrences and fatalities due to tumour. Conclusions: In cases of mesothelioma of the tunica vaginalis testis, the histopathologic markers we chose helped confirm the histo-pathological diagnosis; adequate surgical procedures are typically not curative, and this tumour is often fatal. © 2012 Canadian Urological Association. Source

Guo X.,University of Georgia | Jose P.A.,Center for Molecular Physiology Research | Chen S.-Y.,University of Georgia
American Journal of Physiology - Cell Physiology | Year: 2011

Previous studies demonstrate that response gene to complement 32 (RGC-32) mediates transforming growth factor-β1-induced epithelial-mesenchymal transition (EMT) of human renal proximal tubular cells. However, the mechanisms underlying RGC-32 function remain largely unknown. In the present study, we found that RGC-32 function in EMT is associated with Smad3. Coexpression of RGC-32 and Smad3, but not Smad2, induces a higher mesenchymal marker α-smooth muscle actin (α-SMA) protein expression as compared with RGC-32 or Smad3 alone, while knockdown of Smad3 using short hairpin interfering RNA blocks RGC-32-induced α-SMA expression. These data suggest that RGC-32 interacts with Smad3, but not Smad2, in the regulation of EMT. In addition to α-SMA, RGC-32 and Smad3 also synergistically activate the expression of extracellular matrix protein fibronectin and downregulate the epithelial marker E-cadherin. RGC-32 colocalizes with Smad3 in the nuclei of renal proximal tubular cells. Coimmunoprecipitation assays showed that Smad3, but not Smad2, physically interacts with RGC-32 in renal proximal tubular cells. Mechanistically, RGC-32 and Smad3 coordinate the induction of EMT by regulating the EMT regulators Slug and Snail. Taken together, our data demonstrate for the first time that RGC-32 interacts with Smad3 to mediate the EMT of human renal proximal tubular cells. © 2011 the American Physiological Society. Source

Yang H.,Peking University | Xiong F.X.,Peking University | Lin M.,Peking University | Yang Y.,Center for Molecular Physiology Research | And 2 more authors.
Journal of Cancer Research and Clinical Oncology | Year: 2010

Purpose Lysosomal protein transmembrane 4 beta-35 (LAPTM4B-35) is a tetra-transmembrane glycoprotein that is abundantly localized on membrane-bound organelles including endosomes and lysosomes, and promotes cell proliferation and tumorigenesis through regulation of cell cycle and signaling pathways. The aim of the present study is to determine the potential clinical implications of LAPTM4B-35 expression in hepatocellular carcinoma (HCC). Methods Immunohistochemistry assay was used to determine the expression of LAPTM4B-35 protein in normal and HCC tissues from 71 patients. The correlations of LAPTM4B-35 expression with clinicopathological parameters, including gender, age, background liver, viral status, tumor size, portal vein invasion, histopathological differentiation, serum AFP level, TNM staging and recurrence of HCC were assessed by Chi-squared test. Patient survival and their differences were determined by Kaplan- Meier method and log-rank test. Cox regression (Proportional hazard model) was adopted for multivariate analysis of prognostic factors. Results LAPTM4B-35 immunoreactivity was negative or low in normal liver tissues, but high in HCC tissues (51/71, 71.8%). The overexpression of LAPTM4B-35 was significantly associated with recurrence, TNM staging and portal vein invasion of HCC. Patients with high LAPTM4B-35 expression had significantly poorer overall survival (OS) and disease-free survival (DFS) (both P < 0.001) when compared with patients with the low expression of LAPTM4B-35. On multivariate analysis, LAPTM4B-35 expression was found to be an independent prognostic factor for OS and DFS (P = 0.018 and P = 0.001, respectively). Conclusion LAPTM4B-35 expression showed a strong association with the potencies of recurrence and metastasis and progression of HCC, and that may be applied as a novel marker for the prediction of recurrence and metastasis potency of HCC, and helpful for improving the diagnosis, prognosis and treatment of HCC. © Springer-Verlag 2009. Source

Huang W.-Y.,University of Georgia | Huang W.-Y.,Shanghai JiaoTong University | Huang W.-Y.,Georgetown University | Xie W.,University of Georgia | And 5 more authors.
American Journal of Physiology - Cell Physiology | Year: 2011

Response gene to complement 32 (RGC-32) is activated by transforming growth factor- β (TGF- β) and plays an important role in smooth muscle cell (SMC) differentiation from neural crest Monc-1 cells. The molecular mechanism governing TGF- β activation of RGC-32, however, remains to be determined. The present studies indicate that TGF- β regulates RGC-32 gene transcription. Sequence analysis revealed a Smad binding element (SBE) located in the region from -1344 to -1337 bp upstream of the transcription start site of RGC-32 gene. A polyomavirus enhancer activator (PEA3) binding site is adjacent to the SBE. Mutation at either SBE or PEA3 site significantly inhibited RGC-32 promoter activity. Mutations at both sites completely abolished TGF- β -induced promoter activity. Biochemically, TGF- β stimulated recruitment of Smad2, Smad4, and PEA3 to the RGC-32 promoter, as revealed by gel shift and chromatin immunoprecipitation analyses. Functionally, Smad2, but not Smad3, activated RGC-32 promoter. PEA3 appeared to enhance Smad2 activity. In agreement with their function, Smad2, but not Smad3, physically interacted with PEA3. In TGF- β -induced SMC differentiation of Monc-1 cells, knockdown of Smad2 by short hairpin RNA resulted in downregulation of RGC-32 and SMC marker genes. The downregulation of SMC markers, however, was rescued by exogenously introduced RGC-32. These results demonstrate that Smad2 regulation of RGC-32 transcription is essential for SMC differentiation from neural crest cells. © 2011 the American Physiological Society. Source

Yatabe M.S.,Fukushima Medical University | Yatabe J.,Fukushima Medical University | Watanabe T.,Fukushima Medical University | Felder R.A.,University of Virginia | And 2 more authors.
American Journal of Clinical Nutrition | Year: 2010

Background: The mechanisms by which a derangement of glucose metabolism causes high blood pressure are not fully understood. Objectives: This study aimed to clarify the relation between salt sensitivity of blood pressure and insulin resistance, which are important subcharacteristics of hypertension and impaired glucose metabolism, respectively. Effects on the renin-angiotensin and sympathetic nervous systems were also studied. Design: The state of glucose metabolism was assessed by a hyperinsulinemic euglycemic glucose clamp technique and a 75-g oral-glucose-tolerance test in 24 essential hypertensive patients who were lean and without diabetes or chronic kidney disease. The subjects were classified as salt-sensitive or salt-resistant on the basis of the difference (Δ mean blood pressure ≥5%) between 24-h ambulatory blood pressure monitoring results on the seventh day of low-salt (34 mmol/d) and high-salt (252 mmol/d) diets. Urine and blood samples were collected for analyses. Results: There was a robust inverse relation between the glucose infusion rate (GIR) and the salt sensitivity index. The GIR correlated directly with the change in urinary sodium excretion and was inversely related to the change in hematocrit when the salt diet was changed from low to high, which is indicative of salt and fluid retention in salt-sensitive subjects. The GIR also showed an inverse correlation compared with the changes in urinary norepinephrine excretion, plasma renin activity, and plasma aldosterone concentration. Conclusions: Salt sensitivity of blood pressure is strongly associated with insulin resistance in lean, essential hypertensive patients. Hyperinsulinemia, sympathetic overactivation, and reduced suppression of the renin-angiotensin system may play a role in this relation. © 2010 American Society for Nutrition. Source

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