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Senescent human hepatocytes express a unique secretory phenotype and promote macrophage migration

World Journal of Gastroenterology 2014年第47期20卷 17851-17862页

作者： Katharine M Irvine Richard Skoien Nilesh J Bokil Michelle Melino Gethin P Thomas dorothy Loo Brian Gabrielli Michelle M Hill Matthew J Sweet and.ew d.clouston Elizabeth E Powell Centre for Liver disease Research School of MedicineThe University of QueenslandTranslational Research InstituteBrisbane 4102Australia Institute for Molecular Bio-science The University of QueenslandBrisbane 4067Australia The University of Queensland diamantina Institute The University of Queensland Translational Research InstituteBrisbane 4102Australia department of Gastroenterology and Hepatology Princess Alexandra HospitalBrisbane 4102Australia

AIM: To develop a model of stress-induced senescence to study the hepatocyte senescence associated secretory phenotype (SASP).

关键词： Cell aging Chemokines Hepatocytes Inflammation Liver diseases Macrophages

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Independent effects of diet and exercise training on fat oxidation in non-alcoholic fatty liver disease

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World Journal of Hepatology 2016年第27期8卷 1137-1148页

作者： Ilaria Croci Nuala M Byrne Veronique S Chachay and.ew P Hills and.ew d.clouston Trisha M O'Moore-Sullivan Johannes B Prins Graeme A Macdonald Ingrid J Hickman School of Human Movement and Nutrition Sciences University of Queensland Translational Research Institute the University of Queensland Diamantina Institute Bond Institute of Health and Sport Bond University Institute of Health and Biomedical Innovation Queensland University of Technology School of Health Sciences University of Tasmania Mater Research Institute University of Queensland School of Medi-cine the University of Queensland department of Gastroenterology and Hepatology Princess Alexandra Hospital Translational Research Institute department of Nutrition and dietetics Princess Alexandra Hospital

AIM To investigate the independent effects of 6-mo of dietary energy restriction or exercise training on wholebody and hepatic fat oxidation of patients with nonalcoholic fatty liver disease(NAFLd).METHOdS Participants were randomised into either circuit exercise training(EX;n = 13;3 h/wk without changes in dietary habits),or dietary energy restriction(ER) without changes in structured physical activity(ER;n = 8).Respiratory quotient(RQ) and whole-body fat oxidation rates(Fatox) were determined by indirect calorimetry under basal,insulin-stimulated and exercise *** of disease and steatosis was determined by liver histology;hepatic Fatox was estimated from plasma β-hydroxybutyrate ***;cardiorespiratory fitness was expressed as VO2 ***-case analysis was performed(EX:n = 10;ER:n = 6).RESULTS Hepatic steatosis and NAFLd activity score decreased with ER but not with EX.β-hydroxybutyrate concentrations increased significantly in response to ER(0.08 ± 0.02 mmol/L vs 0.12 ± 0.04 mmol/L,P = 0.03) but remained unchanged in response to EX(0.10 ± 0.03 mmol/L vs 0.11 ± 0.07 mmol/L,P = 0.39).Basal RQ decreased(P = 0.05) in *** EX,while this change was not significant after ER(P = 0.38).VO_(2peak)(P d maximal Fa_(tox) during aerobic exercise(P = 0.03) improved with EX but not with ER(P > 0.05).The increase in β-hydroxybutyrate concentrations was correlated with the reduction in hepatic steatosis(r =-0.56,P = 0.04).CONCLUSION ER and EX lead to specific benefits on fat metabolism of patients with *** hepatic Fat_(ox) in response to ER could be one mechanism through which the ER group achieved reduction in steatosis.

关键词： Non-alcoholic steatohepatitis Steatosis Fat and carbohydrate oxidation Exercise Fitness Beta-hydroxybutyrate Ketone bodies Fatty acid oxidation

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Macrophage secretory products induce an inflammatory phenotype in hepatocytes

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World Journal of Gastroenterology 2012年第15期18卷 1732-1744页

作者： Michelle Melino Victoria L Gadd Gene V Walker Richard Skoien Helen d Barrie dinesh Jothimani Leigh Horsfall Alun Jones Matthew J Sweet Gethin P Thomas and.ew d.clouston Julie R Jonsson Elizabeth E Powell Centre for Liver disease Research School of MedicineThe University of QueenslandPrincess Alexandra HospitalBrisbane 4102QueenslandAustralia department of Gastroenterology and Hepatology Princess Alexandra HospitalBrisbane 4102QueenslandAustralia Institute for Molecular Bioscience and Australian Infectious diseases Research Centre The University of QueenslandBrisbane 4072QueenslandAustralia diamantina Institute The University of QueenslandBrisbane 4102QueenslandAustralia

AIM:To investigate the influence of macrophages on hepatocyte phenotype and ***:Macrophages were differentiated from THP-1 monocytes via phorbol myristate acetate stimulation and the effects of monocyte or macrophageconditioned medium on HepG2 mRNA and protein expression *** in vivo relevance of these findings was confirmed using liver biopsies from 147 patients with hepatitis C virus(HCV)***:Conditioned media from macrophages,but not monocytes,induced a transient morphological change in hepatocytes associated with upregulation of vimentin(7.8±2.5-fold,P=0.045)and transforming growth factor(TGF)-β1(2.6±0.2-fold,Pd downregulation of epithelial cadherin(1.7±0.02-fold,P=0.017)mRNA *** analysis revealed significant upregulation of lipocalin-2(17-fold,P d pathways associated with inflammation,and substantial downregulation of pathways related to hepatocyte *** patients with chronic HCV,realtime polymerase chain reaction and immunohistochemistry confirmed an increase in lipocalin-2 mRNA(F0 1.0 ±0.3,F1 2.2±0.2,F2 3.0±9.3,F3/4 4.0±0.8,P= 0.003)and protein expression(F1 1.0±0.5,F2 1.3± 0.4,F3/4 3.6±0.4,P=0.014)with increasing liver *** performance liquid chromatography-tandem mass spectrometry analysis identified elevated levels of matrix metalloproteinase(MMP)-9 in macrophageconditioned medium,and a chemical inhibitor of MMP-9 attenuated the change in morphology and mRNA expression of TGF-β1(2.9±0.2 vs 1.04±0.1,Pditioned media treated HepG2 *** patients with chronic HCV infection,hepatic mRNA expression of Cd163(F0 1.0±0.2,F1/2 2.8±0.3,F3/4 5.3±1.0,P=0.001)and MMP-9(F0 1.0±0.4,F1/2 2.8±0.3,F3/4 4.1±0.8,P=0.011)was significantly associated with increasing stage of ***:Secreted macrophage products alter the phenotype and function of hepatocytes,with increased expression of inflammatory mediators,suggesting that hepatocytes actively participat

关键词： Macrophages Hepatic fibrosis Lipocalin-2 Transforming growth factor-β1 Matrix metalloproteinase-9

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世界核心医学期刊文摘（胃肠病学分册） 2005年第9期1卷 43-44页

作者： clouston A.d. Powell E.E. Walsh M.J. 杨瑗 Histopath Laboratories Strathfield Plaza Strath-field Sydney 2135 Australia Dr.

The mechanisms for progressive fibrosis and exacerbation by steatosis in patients with chronic hepatitis C (HCV) are still unknown. We hypothesized that proliferative blockade in HCV-infected and steatotic hepatocytes results in the default activation of hepatic progenitor cells (HPC), capable of differentiating into both biliary and hepatocyte lineages, and that the resultant ductular reaction promotes portal fibrosis. To study this concept, 115 liver biopsy specimens from subjects with HCV were scored for steatosis, inflammation, and fibrosis. Biliary epithelium and HPC were decorated by cytokeratin 7 immunoperoxidase, and the replicative state of hepatocytes was assessed by p21 and Ki-67 immunohistochemistry. A ductular reaction at the portal interface was common. There was a highly significant correlation between the area of ductular reaction and fibrosis stage (r = 0.453, P d independently associated after multivariate analysis. HPC numbers also correlated with fibrosis (r = 0.544, P d the ductular area (r = 0.624, P d with greater HPC proliferation (r = 0.372, P = .0004) and ductular reaction (r = 0.374, P d hepatocyte replication by p21 expression was independently associated with HPC expansion (P =.002) and increased with the body mass index (P d lobular inflammation (P = .005). In conclusion, the strong correlation between portal fibrosis and a periportal ductular reaction with HPC expansion, the exacerbation by steatosis, and the associations with impaired hepatocyte replication suggest that an altered regeneration pathway drives the ductular reaction. We believe this triggers fibrosis at the portal tract interface. This may be a stereotyped response of importance in other chronic liver diseases.

关键词：丙肝患者胆管病脂肪变性肝纤维化祖细胞肝细胞系丙肝病毒复制功能肝组织活检肝小叶

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