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cholestasis/protease
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Induction of the mitochondrial permeability transition as a mechanism of liver injury during cholestasis: a potential role for mitochondrial proteases.
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As part of this thematic series on mitochondria in cell death, we would like to review our data on: (1) the role of the mitochondrial permeability transition (MPT) in hepatocyte necrosis during cholestasis; and (2) the concept that endogenous mitochondrial protease activity may lead to the MPT. Many
[Effect of the protease inhibitor contrical on liver and serum proteolytic enzyme activity in experimental cholestasis].
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Effect of bile duct obstruction on pancreatic enzyme secretion and intestinal proteolytic enzyme activity in the rat.
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The role of bile in regulation of intestinal proteolytic activity in rats was investigated by studying the effects of bile diversion and bile duct obstruction on pancreatic protease secretion and on recovery of protease from the intestine. Diversion of bile and pancreatic juice from the intestine
Role of matrix metalloproteinases in cholestasis and hepatic ischemia/reperfusion injury: A review.
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Matrix metalloproteinases (MMPs) are a family of proteases using zinc-dependent catalysis to break down extracellular matrix (ECM) components, allowing cell movement and tissue reorganization. Like many other proteases, MMPs are produced as zymogens, an inactive form, which are activated after their
Defective hepatocyte aquaporin-8 expression and reduced canalicular membrane water permeability in estrogen-induced cholestasis.
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Our previous work supports a role for aquaporin-8 (AQP8) water channels in rat hepatocyte bile formation mainly by facilitating the osmotically driven canalicular secretion of water. In this study, we tested whether a condition with compromised canalicular bile secretion, i.e., the estrogen-induced
Hepatotoxicity of an HIV protease inhibitor in dogs and rats.
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Oral administration of the HIV protease inhibitor L-689,502 caused cholestasis and hepatocyte injury in rats and dogs. These changes occurred rapidly, with elevations in serum transaminase observed as early as 6 hr after oral dosing in dogs. The acute phase of this hepatotoxic response was
Does the mutation of the SERPINA1 gene contribute to liver damage and cholestasis in patients with diagnosed cystic fibrosis? preliminary study.
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Mutation of the SERPINA1 gene is present in about 2% of patients with cystic fibrosis but is more common and accounts for about 5% in patients with cystic fibrosis and co-existing liver lesions. The SERPINA1 gene is responsible for the synthesis of a serine protease inhibitor. The protein related
Alpha1-antitrypsin deficiency in 26-year-old subjects: lung, liver, and protease/protease inhibitor studies.
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BACKGROUND
Clinical and biochemical signs of lung and liver disease have been followed prospectively in a birth cohort of individuals with alpha1-antitrypsin (AAT) deficiency.
OBJECTIVE
At age 26 years, the focus was on clinical health, lung and liver function tests, and plasma markers of the
LPS induces the TNF-alpha-mediated downregulation of rat liver aquaporin-8: role in sepsis-associated cholestasis.
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Although bacterial lipopolysaccharides (LPS) are known to cause cholestasis in sepsis, the molecular mechanisms accounting for this effect are only partially known. Because aquaporin-8 (AQP8) seems to facilitate the canalicular osmotic water movement during hepatocyte bile formation, we studied its
The coagulation system contributes to alphaVbeta6 integrin expression and liver fibrosis induced by cholestasis.
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Chronic injury to intrahepatic bile duct epithelial cells (BDECs) elicits expression of various mediators, including the αVβ6 integrin, promoting liver fibrosis. We tested the hypothesis that tissue factor (TF)-dependent thrombin generation and protease activated receptor-1 (PAR-1) activation
Nuclear serine protease activity contributes to bile acid-induced apoptosis in hepatocytes.
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Glycodeoxycholate (GDC) induces apoptosis in hepatocytes by a mechanism associated with DNA cleavage by endonucleases. In many models of apoptosis, proteolysis is required prior to DNA cleavage. Our aims were to determine if enhanced proteolysis is a mechanism causing GDC-mediated apoptosis. In
Natural protease inhibitors to fibrinolysis in liver diseases.
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The newly discovered alpha 2-antiplasmin and some inhibitors of fibrinolysis were measured in 40 patients with liver diseases. alpha 2-antiplasmin was low in liver cirrhosis, but unchanged in cholestasis when compared with controls.
[Clinical aspects, results of diagnostic pulmonary function tests and biochemical parameters in children with homozygote alpha-1-antitrypsin deficiency].
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The clinical course and pulmonary function tests of individuals with severe Alpha-1-Antitrypsin (Alpha-1-AT) deficiency reveal a marked interindividual variability. 4 patients with PI type ZZ and 2 patients with PI type SZ had been identified by neonatal cholestasis. None had pulmonary symptoms at a
[Alpha 1-antitrypsin deficiency in childhood].
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Alpha-1-antitrypsin is a blood glycoprotein synthesized in the liver. It is a protease inhibitor of the serpine group and has a specific action for elastase. Alpha-1-antitrypsin electrophoresis shows about 20 phenotypes, the normal one being PiM. The allele PiZ is usually responsible for liver or
Bile salt-induced apoptosis of hepatocytes involves activation of protein kinase C.
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Toxic bile salts induce hepatocyte apoptosis, a model relevant to liver injury during cholestasis. However, the signaling mechanisms culminating in bile salt-induced apoptosis remain unclear. Because protein kinase C (PKC) is activated by bile salts in hepatocytes and causes apoptosis in other
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