Affiliation: University of Pennsylvania
- Increased stiffness of the rat liver precedes matrix deposition: implications for fibrosisPenelope C Georges
Dept of Medicine, Univ of Pennsylvania School of Medicine, Philadelphia, PA 19104 6140, USA
Am J Physiol Gastrointest Liver Physiol 293:G1147-54. 2007..We suggest that increased liver stiffness may play an important role in initiating the early stages of fibrosis...
- Autocrine release of TGF-beta by portal fibroblasts regulates cell growthRebecca G Wells
The University of Pennsylvania School of Medicine, 600 CRB 6140, 415 Curie Blvd, Philadelphia, PA 19104 6140, USA
FEBS Lett 559:107-10. 2004..Fibroblast growth factor (FGF)-2, but not platelet derived growth factor (PDGF), causes PF proliferation. These data suggest a mechanism whereby HSC eclipse PF as the dominant myofibroblast population in biliary fibrosis...
- The role of matrix stiffness in hepatic stellate cell activation and liver fibrosisRebecca G Wells
Department of Medicine Gastroenterology, University of Pennsylvania School of Medicine, Philadelphia, PA 19104, USA
J Clin Gastroenterol 39:S158-61. 2005....
- Smad2 and Smad3 play different roles in rat hepatic stellate cell function and alpha-smooth muscle actin organizationMasayuki Uemura
The University of Pennsylvania School of Medicine, Philadelphia, PA 19104, USA
Mol Biol Cell 16:4214-24. 2005..We suggest that TGF-beta, signaling via Smad3, plays an important role in the morphological and functional maturation of hepatic myofibroblasts...
- Repetitive exposure to TGF-beta suppresses TGF-beta type I receptor expression by differentiated osteoblastsKenneth K Kim
Yale University School of Medicine, Department of Surgery, New Haven, CT 06520 8041, USA
Gene 379:175-84. 2006..This tightly controlled system may constitute a feedback loop to protect against TGF-beta excess, and impose important limitations that are required for the progression of events during skeletal growth, remodeling and repair...
- The portal fibroblast: not just a poor man's stellate cellRebecca G Wells
Departments of Medicine GI and Pathology and Laboratory Medicine, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania Electronic address
Gastroenterology 147:41-7. 2014..Understanding the functions of portal fibroblasts will require us to view them as more than just an alternative to hepatic stellate cells in fibrosis. ..
- Isolation of rat portal fibroblasts by in situ liver perfusionJessica W Wen
Division of Gastroenterology, Hepatology and Nutrition, Department of Pediatrics, The Children s Hospital of Philadelphia, Philadelphia, PA, USA
J Vis Exp . 2012..Here, we describe a modified version of the original technique described by Kruglov and Dranoff for isolation of portal fibroblasts from rat liver that results in a relatively pure population of primary cells...
- Cholangiocyte cilia are abnormal in syndromic and non-syndromic biliary atresiaAndrew S Chu
Division of Gastroenterology, Hepatology, and Nutrition, The Children s Hospital of Philadelphia, Philadelphia, PA, USA
Mod Pathol 25:751-7. 2012..Although this may result from severe cholestasis or inflammation, it may also reflect common mechanistic pathways in different forms of BA and may have important implications for understanding the progression of the disease...
- Tissue mechanics and fibrosisRebecca G Wells
The Perelman School of Medicine at the University of Pennsylvania, Philadelphia, PA 19104, USA Electronic address
Biochim Biophys Acta 1832:884-90. 2013..This article is part of a Special Issue entitled: Fibrosis: Translation of basic research to human disease...
- Hepatic stellate cells and portal fibroblasts are the major cellular sources of collagens and lysyl oxidases in normal liver and early after injuryMaryna Perepelyuk
Department of Medicine, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, USA
Am J Physiol Gastrointest Liver Physiol 304:G605-14. 2013..These data suggest a model in which the liver is primed to respond quickly to injury, activating potential mechanical feed-forward mechanisms...
- The role of matrix stiffness in regulating cell behaviorRebecca G Wells
Department of Medicine Gastroenterology, The University of Pennsylvania School of Medicine, Philadelphia, PA, USA
Hepatology 47:1394-400. 2008..Particular mention is made of data suggesting that cells of the liver are mechanosensitive, highlighting the potential importance of these findings in understanding the biology of normal and diseased liver...
- Cellular sources of extracellular matrix in hepatic fibrosisRebecca G Wells
Department of Medicine Gastroenterology, University of Pennsylvania School of Medicine, Philadelphia, PA 19104 6140, USA
Clin Liver Dis 12:759-68, viii. 2008..The future challenge will be to define more explicitly the roles of these different fibrogenic cell populations in fibrosis in a disease-specific way...
- Transforming growth factor-beta and substrate stiffness regulate portal fibroblast activation in cultureZhaodong Li
Department of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA
Hepatology 46:1246-56. 2007....
- Foxl1 is a marker of bipotential hepatic progenitor cells in miceSara D Sackett
Department of Genetics, University of Pennsylvania School of Medicine, Philadelphia, PA, USA
Hepatology 49:920-9. 2009..These results demonstrate that the early Foxl1-Cre lineage cell gives rise to both cholangiocytes and hepatocytes after liver injury and suggest the potential for progenitor-portal fibroblast cell interactions...
- Matrix elasticity, cytoskeletal tension, and TGF-beta: the insoluble and soluble meetRebecca G Wells
Department of Medicine, University of Pennsylvania School of Medicine, Philadelphia, PA 19104, USA
Sci Signal 1:pe13. 2008..More broadly, the work suggests that matrix stiffness could regulate the equilibrium between storage and release of a host of matrix-bound growth factors...
- Hepatic stellate cells require a stiff environment for myofibroblastic differentiationAbby L Olsen
Department of Medicine, University of Pennsylvania School of Medicine, Philadelphia, USA
Am J Physiol Gastrointest Liver Physiol 301:G110-8. 2011..These findings suggest that alterations in liver stiffness are a key factor driving the progression of fibrosis...
- Histologic predictors of fibrosis progression in liver allografts in patients with hepatitis C virus infectionZina Meriden
Department of Pathology and Laboratory Medicine, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania 19104, USA
Clin Gastroenterol Hepatol 8:289-96, 296.e1-8. 2010..Recurrent hepatitis C with ensuing fibrosis is the leading cause of liver allograft loss. We investigated whether histologic features in early posttransplant liver biopsies could predict the rate of fibrosis progression in this population...
- BMP-7: a new TGF-beta family member takes the stage in colitis treatmentRebecca G Wells
The University of Pennsylvania, Philadelphia, Pennsylvania, USA
Inflamm Bowel Dis 10:169. 2004
- Betaglycan inhibits TGF-beta signaling by preventing type I-type II receptor complex formation. Glycosaminoglycan modifications alter betaglycan functionOliver Eickelberg
Department of Pathology, Yale University School of Medicine, New Haven, Connecticut 06520 8019, USA
J Biol Chem 277:823-9. 2002..Our data indicate that betaglycan can function as a potent inhibitor of TGF-beta signaling by a novel mechanism and provide support for an essential but complex role for proteoglycan co-receptors in growth factor signaling...
- Expression of P2Y nucleotide receptors and ectonucleotidases in quiescent and activated rat hepatic stellate cellsJonathan A Dranoff
Yale Univ School of Medicine, Section of Digestive Diseases, 333 Cedar St LMP 1080, New Haven, CT 06520, USA
Am J Physiol Gastrointest Liver Physiol 287:G417-24. 2004..Because activation of P2Y receptors in activated HSC regulates procollagen-1 transcription, P2Y receptors may be an attractive target to prevent or treat liver fibrosis...
- Smads 2 and 3 are differentially activated by transforming growth factor-beta (TGF-beta ) in quiescent and activated hepatic stellate cells. Constitutive nuclear localization of Smads in activated cells is TGF-beta-independentChenghai Liu
Department of Internal Medicine, Yale University School of Medicine, New Haven, Connecticut 06520, USA
J Biol Chem 278:11721-8. 2003..These results demonstrate essential differences between TGF-beta-mediated signaling pathways in quiescent and in vitro transdifferentiated hepatic stellate cells...
- Betaglycan as a modulator of TGF-beta signaling in hepatomaRebecca Wells; Fiscal Year: 2008..They will also greatly increase our understanding of TGF-beta signaling in general, and will pave the way for in vivo studies of beta glycan. ..