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hypertrophy/proline
Länken sparas på Urklipp
Sida 1 från 209 resultat
Bile duct enlargement by infusion of L-proline: potential significance in biliary atresia.
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The normal signals of control of bile duct morphogenesis and growth are unknown. Consequently, aberrant development is poorly understood, as for example in those infants with biliary atresia or hypoplasia. A previous report by Isseroff et al., showed that a possible mechanism for the common bile
Protocollagen proline hydroxylase activity in work-induced hypertrophy of rat muscle.
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Protocollagen proline hydroxylase activity in rat heart during experimental cardiac hypertrophy.
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Fascioliasis: role of proline in bile duct hyperplasia.
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In animals fascioliasis, extensive hyperplasia of the main bile duct occurs that often results in enlargement of the duct to more than 20 times the normal. We report that proline infused into the abdominal cavity of rats caused hyperplasia of the bile duct resembling that produced in the early
Tumor suppressor A20 protects against cardiac hypertrophy and fibrosis by blocking transforming growth factor-beta-activated kinase 1-dependent signaling.
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A20 or tumor necrosis factor-induced protein 3 is a negative regulator of nuclear factor kappaB signaling. A20 has been shown previously to attenuate cardiac hypertrophy in vitro and postmyocardial infarction remodeling in vivo. In the present study, we tested the hypothesis that overexpression of
Induction of salivary polypeptides associated with parotid hypertrophy by gallotannins administered topically into the mouse mouth.
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Isoproterenol-induced salivary polypeptides (IISP), a group of proline-rich proteins synthesized by mouse parotids, have been considered as markers for isoproterenol-induced parotid hypertrophy. Rodents fed diets containing high-tannin cereals (sorghum), also develop parotid hypertrophy. To test
Focal adhesion kinase and p130Cas mediate both sarcomeric organization and activation of genes associated with cardiac myocyte hypertrophy.
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Hypertrophic terminally differentiated cardiac myocytes show increased sarcomeric organization and altered gene expression. Previously, we established a role for the nonreceptor tyrosine kinase Src in signaling cardiac myocyte hypertrophy. Here we report evidence that p130Cas (Cas) and focal
Inhibition of Apoptosis Signal-Regulating Kinase 1 Attenuates Myocyte Hypertrophy and Fibroblast Collagen Synthesis.
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BACKGROUND
Cardiac remodelling is a dynamic process whereby structural and functional changes occur within the heart in response to injury or inflammation. Recent studies have demonstrated reactive oxygen species sensitive MAPK, apoptosis signal-regulating kinase 1 (ASK1) plays a critical role in
Isoproterenol-mediated parotid gland hypertrophy is inhibited by effectors of 4 beta-galactosyltransferase.
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Chronic administration of the beta-adrenergic receptor agonist isoproterenol results in parotid gland hypertrophy and hyperplasia. This physiological change in the gland has recently been reported to be accompanied by a dramatic increase in the rate of synthesis and accumulation of the enzyme 4
Role of N-acetyl-seryl-aspartyl-lysyl-proline in the antifibrotic and anti-inflammatory effects of the angiotensin-converting enzyme inhibitor captopril in hypertension.
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Angiotensin-converting enzyme inhibitors (ACEis) are known to have antifibrotic effects on the heart and kidney in both animal models and humans. N-acetyl-seryl-aspartyl-lysyl-proline is a natural inhibitor of proliferation of hematopoietic stem cells and a natural substrate of ACEi that was
Prevention of aortic fibrosis by N-acetyl-seryl-aspartyl-lysyl-proline in angiotensin II-induced hypertension.
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Fibrosis is an important component of large conduit artery disease in hypertension. The endogenous tetrapeptide N-acetyl-seryl-aspartyl-lysyl-proline (Ac-SDKP) has anti-inflammatory and antifibrotic effects in the heart and kidney. However, it is not known whether Ac-SDKP has an anti-inflammatory
The effects of high glucose concentration on angiotensin II- or transforming growth factor-beta-induced DNA synthesis, hypertrophy and collagen synthesis in cultured rat mesangial cells.
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Hyperglycemia is a principal characteristic of diabetes, and has an influence on many cellular functions. In order to investigate whether the intracellular signaling pathways inducing proliferation, hypertrophy and matrix synthesis of mesangial cells are altered in a diabetic environment, we
Prevention of collagen deposition following pulmonary oxygen toxicity in the rat by cis-4-hydroxy-L-proline.
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Exposure of rats to high oxygen tensions causes increased collagen content of lungs and alveolar enlargement in 3-6 wk. We tested whether cis-hydroxyproline, a proline analogue that inhibits collagen synthesis, could prevent the collagen accumulation and alveolar enlargement. Rats were exposed to
General pharmacology of the non-sulfhydryl angiotensin converting enzyme inhibitor N-[8-amino-1(S)-carboxyoctyl]-L-alanyl-L-proline.
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The effects of N-[8-amino-1(S)-carboxyoctyl]-L-alanyl-L-proline (AB-47, CAS 120008-53-9), an orally active angiotensin converting enzyme inhibitor, on the central nervous, respiratory and cardiovascular, autonomic systems, isolated smooth muscles and other functions were investigated in various
Antifibrotic effects of N-acetyl-seryl-aspartyl-Lysyl-proline on the heart and kidney in aldosterone-salt hypertensive rats.
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N-acetyl-seryl-aspartyl-lysyl-proline (Ac-SDKP) inhibits not only hematopoietic cell proliferation but also fibroblast proliferation and collagen synthesis in vitro. Ac-SDKP also prevents collagen deposition and cell proliferation in the left ventricle (LV) in rats with renovascular hypertension
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