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of 66
pro vyhledávání: '"Michael J. P. Arthur"'
Publikováno v:
Journal of gastroenterology and hepatology. 13(S1)
Hepatic stellate cells (HSC) play a central role in the pathogenesis of liver fibrosis. Following liver injury, these cells proliferate and are activated to a profibrogenic myofibroblastic phenotype. In addition to increased matrix protein synthesis,
Autor:
John P. Iredale, Hideaki Nagase, Frank Murphy, Razao Issa, Xiaoying Zhou, Michael J. P. Arthur, Christopher Benyon, Shabna Ratnarajah
Publikováno v:
Journal of Biological Chemistry. 277:11069-11076
The activated hepatic stellate cell (HSC) is central to liver fibrosis as the major source of collagens I and III and the tissue inhibitors of metalloproteinase-1 (TIMP-1). During spontaneous recovery from liver fibrosis, there is a decrease of TIMP
Autor:
Mark Harris, Derek A. Mann, David E. Smart, Frank Murphy, Christopher McCormick, Runping Gao, Fiona Oakley, Richard Ruddell, Michael J. P. Arthur
Publikováno v:
Liver. 22:15-22
Background/aims: Gene transfer into hepatic stellate cells (HSC) is inefficient when using plasmid-based transfection methods; viral-based systems are therefore being developed. A baculovirus system has recently been shown to be useful for expressing
Autor:
Finn Larsen, Robert Sutton, Michael J. P. Arthur, Cornel C. Sieber, Daniel Grandt, Peter Schiedermaier, Phillip Harrison, Jürgen Drewe
Publikováno v:
Digestion. 65:56-60
Background: Lanreotide, a new long-acting somatostatin analogue, has been shown to inhibit the meal-stimulated increase of splanchnic blood flow in healthy volunteers. To date, similar data in patients with liver cirrhosis have not been available. We
Autor:
Julie E. Trim, David E. Smart, Karen J. Vincent, Michael J. P. Arthur, Erick C. Jones, Matthew C. Wright, Derek A. Mann
Publikováno v:
Gut. 49:713-719
BACKGROUND—Activation of hepatic stellate cells (HSCs) to a myofibroblastic phenotype is a key event in liver fibrosis. Identification of transcription factors with activities that are modulated during HSC activation will improve our understanding
Autor:
Elizabeth J. Williams, B H Grove, RC Benyon, John P. Iredale, E N Unemori, Michael J. P. Arthur, R Hadwin, Nathan Trim
Publikováno v:
Gut. 49:577-583
BACKGROUND—Following liver injury, hepatic stellate cells (HSC) transform into myofibroblast-like cells (activation) and are the major source of type I collagen and the potent collagenase inhibitors tissue inhibitors of metalloproteinases 1 and 2 (
Autor:
David E. Smart, Jelena Mann, Oliver Eickelberg, Marc Castellazzi, Karen J. Vincent, Michael J. P. Arthur, Derek A. Mann
Publikováno v:
Journal of Biological Chemistry
Journal of Biological Chemistry, 2001, 276, pp.24414-24421
Journal of Biological Chemistry, 2001, 276, pp.24414-24421
Activation of hepatic stellate cells (HSCs) to a myofibroblast-like phenotype is the pivotal event in hepatic wound healing and fibrosis. Rat HSCs activated in vitro express JunD, Fra2, and FosB as the predominant AP-1 DNA-binding proteins, and all t
Autor:
Michael J. P. Arthur
Publikováno v:
American Journal of Physiology-Gastrointestinal and Liver Physiology. 279:G245-G249
Liver fibrosis is characterized by activation of hepatic stellate cells, which are then involved in synthesis of matrix proteins and in regulating matrix degradation. In the acute phases of liver injury and as liver fibrosis progresses, there is incr
Autor:
David R. Brigstock, Marianna D. A. Gaça, Elizabeth J. Williams, Michael J. P. Arthur, R. Christopher Benyon
Publikováno v:
Journal of Hepatology. 32:754-761
Background/Aims: Connective tissue growth factor is a recently described mitogenic protein implicated in a variety of fibrotic disorders. Connective tissue growth factor may be a downstream mediator of the pro-fibrotic and mitogenic actions of transf
Autor:
John P. Iredale, R. Christopher Benyon, Christopher J. Hovell, Marianna D. A. Gaça, Michael J. P. Arthur, Emma H. Jones
Publikováno v:
Hepatology. 30:977-986
Activated hepatic stellate cells (HSCs) are a potential source of gelatinase A, which accumulates in fibrotic livers. Progelatinase A activation requires its binding to a complex of membrane-type matrix metalloproteinase (MT-MMP) and tissue inhibitor