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Σελίδα 1 από 682 Αποτελέσματα
Effects of HIV protease inhibitors on progression of monocrotaline- and hypoxia-induced pulmonary hypertension in rats.
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BACKGROUND
Pulmonary hypertension (PH) is among the complications of HIV infection. Combination antiretroviral therapy may influence the progression of HIV-related PH. Because Akt signaling is a potential molecular target of HIV protease inhibitors (HPIs), we hypothesized that these drugs altered
Growth and protease secretion of Scedosporium aurantiacum under conditions of hypoxia.
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One of the micro-environmental stresses that fungal pathogens, such as Scedosporium aurantiacum, colonising human lungs encounter in vivo is hypoxia, or deficiency of oxygen. In this work, we studied the impacts of a hypoxic micro-environment (oxygen levels ≤1%) on the growth of a clinical S.
Histochemical investigation of myocardial proteases in heart anoxia, under protection with cardioplegic solution and protease inhibitors.
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We studied the histochemical behaviour of neutral non-lysosomal and acid lysosomal proteases of the myocardium in heart anoxia by aorta-clamping, using an experimental model alike to the open heart surgery conditions. After one hour of blood deprivation we found destabilization, conglomeration,
Serine protease inhibitors suppress cytochrome c-mediatedcaspase-9 activation and apoptosis during hypoxia-reoxygenation.
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We have shown that reoxygenation of hypoxic rat kidney proximaltubule cells leads to apoptosis. This is mediated by translocation ofBax from the cytosol to mitochondria, accompanied by release ofmitochondrial cytochrome c (cyt.c). The present studyhas examined the proteolytic mechanisms responsible
Calpain protease causes hypoxia-induced proteolysis in cultured human retina.
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OBJECTIVE
Calpain proteases are known to be involved in retinal cell death in animal models. The purpose of the present study was to test for calpain activation in human retinas cultured under hypoxic conditions.
METHODS
Calpain activation was detected by immunoblotting for calpain substrates in
Neuroprotective effect of protease-activated receptor-2 in the hypoxia-induced apoptosis of rat RGC-5 cells.
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Hypoxia-induced apoptosis of retinal ganglion cells (RGCs) is regarded as a pivotal pathological process in various ocular diseases. Protease-activated receptor-2 (PAR-2) is involved in the regulation of cell inflammation, differentiation, and apoptosis in many cell types and tissues, but the role
The role of cysteine proteases in hypoxia-induced rat renal proximal tubular injury.
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The role of the lysosomal proteases cathepsins B and L and the calcium-dependent cytosolic protease calpain in hypoxia-induced renal proximal tubular injury was investigated. As compared to normoxic tubules, cathepsin B and L activity, evaluated by the specific fluorescent substrate
Hypoxia down-regulates expression of secretory leukocyte protease inhibitor in bronchial epithelial cells via TGF-β1.
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BACKGROUND
Secretory leukocyte protease inhibitor (SLPI) is a protein with anti-protease and antimicrobial properties that is constitutively secreted from the airway epithelium. The importance of maintaining a balance between proteases and anti-proteases, and robust innate defence mechanisms in the
Lack of apoptotic protease activating factor-1 expression and resistance to hypoxia-induced apoptosis in cervical cancer.
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OBJECTIVE
Clinical observations suggest that intratumoral hypoxia increases the aggressiveness of tumors through clonal selection of cancer cells that have lost their apoptotic potential. The aim of this study, therefore, was to investigate the expression of the proapoptotic protein apoptotic
The role of calcium activated neutral protease on myocardial cell injury in hypoxia.
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The aim of this study was to investigate the correlation between hypoxic myocardial cell injury and intracellular protease activity. Cardiac myocytes were isolated from neonatal rat hearts and cultured in Eagle's modified minimum essential medium. Myocytes were incubated in hypoxic conditions for 6
Effects of thiol protease inhibitors on fodrin degradation during hypoxia in cultured myocytes.
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The effects of thiol protease inhibitors on fodrin (a cell membrane nonerythroid spectrum-like protein) degradation were studied during hypoxia in cultured myocytes. Cardiac myocytes, isolated from neonatal rat hearts, were incubated under hypoxic conditions for 6 h. Cell membrane proteins,
A Ca(2+)-dependent cysteine protease is associated with anoxia-induced root tip death in maize.
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Imposition of anoxia on maize (Zea mays cv. B73) seedlings for 48 h or longer led to the death of the root tip. The necrosis extended into the root axis during postanoxic treatment, leading to the mortality of 30-50% of the seedlings. Using zymography, protease profiles in the root tissues of anoxic
Role of protease activated receptor 1 and 2 signaling in hypoxia-induced angiogenesis.
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OBJECTIVE
Tissue factor (TF) initiates coagulation and indirectly triggers thrombin-dependent protease activated receptor (PAR) signaling. The TF-VIIa complex also directly cleaves PAR2 and promotes angiogenesis in vitro in TF cytoplasmic domain-deleted (TF(deltaCT)) mice. Here we address the effect
Hypoxia Triggers SENP1 (Sentrin-Specific Protease 1) Modulation of KLF15 (Kruppel-Like Factor 15) and Transcriptional Regulation of Arg2 (Arginase 2) in Pulmonary Endothelium.
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OBJECTIVE
KLF15 (Kruppel-like factor 15) has recently been shown to suppress activation of proinflammatory processes that contribute to atherogenesis in vascular smooth muscle, however, the role of KLF15 in vascular endothelial function is unknown. Arginase mediates inflammatory vasculopathy and
SUMO-specific protease 1 is essential for stabilization of HIF1alpha during hypoxia.
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SUMOylation is a dynamic process, catalyzed by SUMO-specific ligases and reversed by Sentrin/SUMO-specific proteases (SENPs). The physiologic consequences of SUMOylation and deSUMOylation are not fully understood. Here we investigate the phenotypes of mice lacking SENP1 and find that SENP1(-/-)
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