proteinase inhibitor/necrosis

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Relation between tumor necrosis factor-alpha and granulocyte elastase-alpha 1-proteinase inhibitor complexes in the plasma of patients with cystic fibrosis.

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Patients with cystic fibrosis suffer from a chronic, progressively destructive bronchitis characterized by colonization of the airways by Pseudomonas aeruginosa. Cell wall lipopolysaccharides from P. aeruginosa may stimulate secretion of cytokines such as tumor necrosis factor alpha (TNF alpha) by

Acute hemorrhagic pancreatic necrosis in mice. Effects of proteinase inhibitors on its induction.

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An acute hemorrhagic pancreatitis with fat necrosis (AHPN) was induced in female mice fed a choline-deficient diet containing 0.5% DL-ethionine. The effect of various proteinase inhibitors on the induction of the pancreatitis was evaluated using three parameters, the mortality of the animals, the

Photodynamic therapy combined with a cysteine proteinase inhibitor synergistically decrease VEGF production and promote tumour necrosis in a rat mammary carcinoma.

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OBJECTIVE Photodynamic therapy (PDT) and inhibition of cathepsin B proteases by cystatin (cysteine proteinase inhibitor, CPI) are potential new tumour treatment modalities. We have investigated the efficacy of PDT and CPI alone and in combination on a solid mammary carcinoma transplanted into Wistar

Relation between tumor necrosis factor-alpha and granulocyte elastase-alpha 1-proteinase inhibitor complexes in the plasma of patients with cystic fibrosis.

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[Treatment of pancreatic necrosis and pancreatitis using a proteinase inhibitor (Trasylol)].

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Plasminogen activator inhibitor type 2 inhibits tumor necrosis factor alpha-induced apoptosis. Evidence for an alternate biological function.

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Plasminogen activator inhibitor type 2 (PAI-2) is a serine proteinase inhibitor or serpin that is a major product of macrophages in response to endotoxin and inflammatory cytokines. We have explored the role of PAI-2 in apoptotic cell death initiated by tumor necrosis factor alpha (TNF). HeLa cells

Extracellular proteinase inhibitor-accelerated apoptosis is associated with B cell activating factor in mammary epithelial cells.

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The expression of extracellular proteinase inhibitor (Expi) gene was induced during the involution of mammary gland, when apoptosis occurs in this tissue. Transient transfection of Expi gene partially induced apoptosis of mammary epithelial HC11 cells. We developed the stable cell lines

Secretion of protease nexin-II/amyloid beta protein precursor by human colorectal carcinoma cells and its modulation by cytokines/growth factors and proteinase inhibitors.

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Trypsin inhibitors secreted by human colorectal adenocarcinoma cell lines were analyzed by reverse zymography. Among eleven cell lines analyzed, the major inhibitor secreted was protease nexin-II (PN-II), a secreted form of amyloid beta protein precursor (APP) containing a Kunitz-type serine

Platelet-activating factor biosynthesis by cultured mesangial cells is modulated by proteinase inhibitors.

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Rat mesangial cells stimulated with calcium ionophore A23187 and phagocytosis were shown to produce platelet-activating factor (PAF), a mediator of inflammation and endotoxic shock. In the study presented here, the cultured human mesangial but not epithelial cells synthetized PAF not only in

Tumor necrosis factor increases the elastolytic potential of adherent neutrophils: a role for hypochlorous acid.

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Neutrophils adhered to biologic surfaces exhibit proteolytic cleavage of surface proteins even in the presence of proteinase inhibitors. Such proteolysis is restricted to the pericellular space and appears to require the dual action of proteinases and reactive oxygen species. The present study was

Proteinase inhibitor 6 cannot be secreted, which suggests it is a new type of cellular serpin.

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We have recently described a new serine proteinase inhibitor, proteinase inhibitor 6 (PI-6). This serpin has features that suggest it may function intracellularly, but its close resemblance to ovalbumin serpins like plasminogen activator inhibitor 2 (PAI-2) raises the possibility that it is secreted

Pancreatitis with arthropathy and subcutaneous fat necrosis. Evidence for the pathogenicity of lipolytic enzymes.

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The occurrence of peripheral fat necrosis in exceptional cases of pancreatic disease is not well understood. We report studies on such a patient with arthropathy and subcutaneous nodules. Examination of serial serum samples demonstrated striking elevations of the pancreatic enzymes phospholipase A,

Structure-activity relationship of hydroxamate-based inhibitors on the secretases that cleave the amyloid precursor protein, angiotensin converting enzyme, CD23, and pro-tumor necrosis factor-alpha.

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Multiple proteins are proteolytically shed from the membrane, including the amyloid precursor protein (APP) involved in Alzheimer's disease, the blood pressure regulating angiotensin converting enzyme (ACE), the low affinity IgE receptor CD23, and the inflammatory cytokine tumor necrosis

Apoptosis-inducing agents cause rapid shedding of tumor necrosis factor receptor 1 (TNFR1). A nonpharmacological explanation for inhibition of TNF-mediated activation.

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Several chemical compounds not known to interact with tumor necrosis factor (TNF) signal transducing proteins inhibit TNF-mediated activation of vascular endothelial cells (EC). Four structurally diverse agents, arachidonyl trifluoromethylketone, staurosporine, sodium salicylate, and C6-ceramide,

Constitutive and regulated secretion of secretory leukocyte proteinase inhibitor by human intestinal epithelial cells.

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OBJECTIVE Epithelial cells participate in immune regulation and mucosal integrity by generating a range of biologically active mediators. In the intestine, little is known about the potential endogenous anti-inflammatory molecules. Secretory leukocyte proteinase inhibitor (SLPI) is a major serine

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