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Clinical significance of mucosal suppressors of cytokine signaling 3 expression in ulcerative colitis

World Journal of Gastroenterology 2007年第21期13卷 2939-2944页

作者： Yoshihiro Miyanaka Yoshitaka Ueno Shinji Tanaka Kyoko Yoshioka Tsuyoshi Hatakeyama Masaru Shimamoto Masaharu Sumii Kazuaki Chayama Department of Medicine and Molecular Science Hiroshima UniversityHiroshimaJapan Department of Endoscopy Hiroshima University HospitalHiroshimaJapan Department of Internal Medicine Hiroshima Memorial HospitalJapan

AIM:To investigate the clinical significance of mucosal expression of suppressors of cytokine signaling 1 (SOCS1) and SOCS3 in human ulcerative colitis (UC). METHODS:Biopsy specimens for histological analysis and mRNA detection were obtained endoscopically from the rectum of 62 patients with UC (36 men; age 13-76 years). The patients were classified endoscopically according to Matts' grade (grade 1 to 4). Expression of SOCS1 and SOCS3 mRNAs was quantified in samples by competitive reverse transcription-polymerase chain reaction (RT-PCR). GAPDH was used as an internal control for efficiency of RT-PCR and amount of RNA. RESULTS:SOCS3 mRNA expression was significantly higher in inflamed mucosa of UC than in inactive mucosa. The level of expression was well correlated with the degree of both endoscopic and histologic inflammation. Interestingly,among the patients in remission,the group with relatively low expression of SOCS3 showed a higher rate of remission maintenance over a 12-mo period. In contrast,SOCS1 mRNA was expressed in both inflamed and non-inflamed colonic mucosa and was not correlated with the activity of colonic mucosa or prognosis. CONCLUSION:These observations suggest that increased expression of mucosal SOCS3,but not of SOCS1,may play a critical role in the development of the colonic inflammation of UC.

关键词： suppressors of cytokine signaling Ulcerative colitis

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Ron receptor-dependent gene regulation in a mouse model of endotoxin-induced acute liver failure

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Hepatobiliary & Pancreatic Diseases International 2012年第4期11卷 383-392页

作者： Rishikesh M Kulkarni Louis W Kutcher William D Stuart Daniel J Carson Mike A Leonis Susan E Waltz Departments of Cancer and Cell Biology University of CincinnatiCincinnatiOH 45267-0521USA Biology University of CincinnatiCincinnatiOH 45267-0521USA Division of Gastroenterology Hepatology and NutritionCincinnati Children's Hospital Medical CenterCincinnatiOH 45229USA Department of Research Shriner's Hospital for Children and Cincinnati Veterans Affairs Medical CenterCincinnatiOH 45267-0521USA

BACKGROUND:Prior experimentation has shown that loss of the tyrosine kinase(TK) signaling domain of the Ron receptor leads to marked hepatocyte protection in a model of lipopolysaccharideinduced acute liver failure(ALF) in D-galactosamine(GalN)sensitized *** aim of this study was to identify the role of Ron in the regulation of hepatic gene ***:Microarray analyses were performed on liver RNA isolated sequentially from wild-type(WT) and TK-/mice during the progression of *** array data were validated using Western and immunohistochemistry analyses as well as with ex vivo culture ***:At baseline,101 genes were differentially expressed between WT and TK-/-livers,which regulate processes involved in hypoxia,proliferation,apoptosis and *** hour after ALF induction,WT livers exhibited increased cytokine expression compared to TK-/-livers,and after 4 hours,an induction of suppressor of cytokine signaling(SOCS) genes as well as JAK-STAT pathway activation were prominent in TK-/livers compared to ***:Our studies suggest a novel hepato-protective mechanism in Ron TK-/-mice wherein increased and sustained SOCS production and JAK-STAT activation in the hepatocyte may inhibit the destructive proinflammatory milieu and promote survival factors which blunt hepatic death and the ensuing development of ALF.

关键词： Mst1R suppressors of cytokine signaling Met receptor hepatocyte growth factor-like protein

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Pathophysiology of insulin resistance and steatosis in patients with chronic viral hepatitis

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World Journal of Gastroenterology 2011年第36期17卷 4055-4062页

作者： Metin Basaranoglu Gkcen Basaranoglu Division of Gastroenterology and Hepatology Teaching and ConsultingAnkara Yüksek Ihtisas Hospital Gastroenterology ClinicSihhiyeAnkara 06100Turkey Department of Anaesthesiology Bezmialem Vakif UniversityFatihIstanbul 34590Turkey

Chronic hepatitis due to any cause leads to cirrhosis and end-stage liver disease.A growing body of literature has also shown that fatty liver due to overweight or obesity is a leading cause of *** to the obesity epidemic,fatty liver is now a significant problem in clinical *** has an impact on the acceleration of liver damage in patients with chronic hepatitis due to other *** association between hepatitis C virus (HCV) infection,steatosis and the onset of insulin resistance has been *** resistance is one of the leading factors for severe fibrosis in chronic HCV ***,hyperinsulinemia has a deleterious effect on the management of chronic *** to therapy is increased by decreasing insulin resistance by weight loss or the use of thiazolidenediones or *** underlying mechanisms of this complex interaction are not fully understood.A direct cytopathic effect of HCV has been *** genomic structure of HCV (suggesting that some viral sequences are involved in the intracellular accumulation of triglycerides),lipid metabolism,the molecular links between the HCV core protein and lipid droplets (the core protein of HCV and its transcriptional regulatory function which induce a triglyceride accumulation in hepatocytes) and increased neolipogenesis and inhibited fatty acid degradation in mitochondria have been investigated.

关键词： Adipocytokines Fatty acids Hepatitis B virus Hepatitis C virus Inducible nitric oxide synthase Insulin resistance Signal transduction and activator of transcription-3 Steatosis Sterol regulatory elementbinding protein-1c suppressors of cytokine signaling Tumor necrosis factor-α

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