Affiliation: University of North Carolina
- Favored T helper 1 response in a mouse model of hepatosteatosis is associated with enhanced T cell-mediated hepatitisMichael Kremer
Center for Alcohol Studies, The University of North Carolina at Chapel Hill, NC 27599, USA
Hepatology 44:216-27. 2006..In conclusion, these data support the hypothesis that hepatosteatosis caused by CDD is associated with more severe ConA-induced hepatitis due to a predominant shift toward Th1 response...
- Pivotal role of Smad3 in a mouse model of T cell-mediated hepatitisMichael Kremer
Center for Alcohol Studies, University of North Carolina, Chapel Hill, NC 27599, USA
Hepatology 47:113-26. 2008..In vitro, Smad3(-/-) hepatocytes were resistant to TGFbeta-induced apoptosis, and this protection was dependent on extracellular signal-regulated kinase activation...
- Impaired liver regeneration and increased oval cell numbers following T cell-mediated hepatitisIan N Hines
Center for Alcohol Studies, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA
Hepatology 46:229-41. 2007..Finally, splenocytes isolated from ConA-pretreated mice exerted cytotoxicity toward autologous bone marrow cells in an NK cell-dependent manner...
- Kupffer cell and interleukin-12-dependent loss of natural killer T cells in hepatosteatosisMichael Kremer
Center for Alcohol Studies, University of North Carolina at Chapel Hill, NC 27599, USA
Hepatology 51:130-41. 2010..Finally, human livers with severe steatosis showed a substantial decrease in NKT cells...
- LPS signaling enhances hepatic fibrogenesis caused by experimental cholestasis in miceFuyumi Isayama
Laboratory of Hepatobiology and Toxicology, Department of Pharmacology, University of North Carolina, Chapel Hill, 27599, USA
Am J Physiol Gastrointest Liver Physiol 290:G1318-28. 2006..In conclusion, these data demonstrate that endotoxin in a CD14-dependent manner exacerbates hepatic fibrogenesis and macrophage activation to produce oxidants and cytokines after bile duct ligation...
- Extrahepatic cells contribute to the progenitor/stem cell response following reduced-size liver transplantation in miceLars O Conzelmann
Laboratory of Hepatobiology and Toxicology, Center for Alcohol Studies, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA
Exp Biol Med (Maywood) 232:571-80. 2007..Reduced-size liver transplantation using GFP(+) transgenic mice supports the hypothesis that recipient-derived progenitor cells are present and may contribute to liver regeneration following transplantation...
- Natural killer T cells and non-alcoholic fatty liver disease: fat chews on the immune systemMichael Kremer
Department of Surgery, University of Heidelberg, Heidelberg, Germany
World J Gastroenterol 14:487-8. 2008....
- Graft tumor necrosis factor receptor-1 protects after mouse liver transplantation whereas host tumor necrosis factor receptor-1 promotes injuryLars O Conzelmann
Department of Cell and Developmental Biology, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA, and Department of Trauma, Hand and Reconstructive Surgery, Hospitals of the J W Goethe University, Frankfurt, Germany
Transplantation 82:1214-20. 2006..TNFR1 mediates liver injury after ischemia/reperfusion but is also mitogenic during hepatic regeneration. This study investigated the role of graft and host TNFR1 in early graft injury after liver transplantation in mice...
- Smad3 signaling in the regenerating liver: implications for the regulation of IL-6 expressionMichael Kremer
Department of General Surgery, University of Ulm, Ulm, Germany Department of Medicine, Division of Gastroenterology and Hepatology, University of North Carolina, Chapel Hill, NC, USA
Transpl Int 27:748-58. 2014..Therapies directed at finely regulating Smad3 activation early within the regenerating liver may prove useful in promoting liver cell proliferation and restoration of liver mass...
- Development and functional consequences of LPS tolerance in sinusoidal endothelial cells of the liverAnja Uhrig
Department of Transplant Surgery, University Mainz, Germany
J Leukoc Biol 77:626-33. 2005..Our results support the notion that LPS tolerance in organ-resident scavenger LSEC contributes to local hepatic control of inflammation...
- Identification of differentially expressed genes after partial rat liver ischemia/reperfusion by suppression subtractive hybridizationChristine Fallsehr
Institute of Molecular Pathology, University of Heidelberg, Heidelberg, Germany
World J Gastroenterol 11:1303-16. 2005..To identify potential diagnostic target genes in early reperfusion periods following warm liver ischemia before irreversible liver damage occurs...