hydroxylysine/enflamasyon

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Sayfa 1 itibaren 18 Sonuçlar

Urinary excretion of hydroxylysyl glycosides during acute inflammation in the rat.

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1. Subcutaneous inflammatory granuloma were induced in young rats and the urinary excretion of hydroxyproline and hydroxylysyl glycosides was observed during the period of acute inflammation. 2. All collagen metabolites were increased in the urine and excretion of glucosyl-galactosyl-hydroxylysine

Inflammation-associated lysyl oxidase protein expression in vivo, and modulation by FGF-2 plus IGF-1.

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Lysyl oxidase is the extracellular enzyme that catalyzes oxidative deamination of peptidyl-lysine residues in elastin precursors, and lysine and hydroxylysine residues in collagen precursors to form peptidyl-aldehydes. These aldehydes then spontaneously condense to crosslink collagen and elastin and

Down-regulation of GLT25D1 inhibited collagen secretion and involved in liver fibrogenesis.

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Collagen β (1-O) galactosyltransferase 1 (GLT25D1) has been reported to transfer galactose to hydroxylysine residues via β (1-O) linkages in collagen. However, the role of Glt25d1 in liver fibrogenesis is still unknow. Recently, we generated a Glt25d1 knockout mouse to elucidate the role of Glt25d1

Alveolar macrophage modulation of proteolysis by neutrophil elastase in extracellular matrix.

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An extracellular connective tissue matrix, made up of components found in the pulmonary alveolar interstitium, was generated in vitro and used as a culture surface and substrate for proteolysis by human alveolar macrophages (AM) and neutrophil elastase (NE). The ability of human AM to modulate

Interleukin 4 and prolonged hypoxia induce a higher gene expression of lysyl hydroxylase 2 and an altered cross-link pattern: important pathogenetic steps in early and late stage of systemic scleroderma?

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The major pathological processes of systemic scleroderma (SSc) comprise inflammation and microvascular damage in the early or acute progressive stage as well as tissue fibrosis and hypoxia in the chronic end stage. Fibrosis seems to be a general phenomenon characterized by an increase of

Laser induced wounds and scarring modified by antiinflammatory drugs: a murine model.

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Scarring is a well-known side effect to cutaneous laser treatment. Therefore we investigated if wounds and scarring could be decreased by pharmacological interference in the acute inflammatory reaction following laser therapy. A copper vapor laser operating at 578 nm was used at three different

Human 2-Oxoglutarate Dehydrogenase and 2-Oxoadipate Dehydrogenase Both Generate Superoxide/H2O2 in a Side Reaction and Each Could Contribute to Oxidative Stress in Mitochondria.

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According to recent findings, the human 2-oxoglutarate dehydrogenase complex (hOGDHc) could be an important source of the reactive oxygen species in the mitochondria and could contribute to mitochondrial abnormalities associated with multiple neurodegenerative diseases, including Alzheimer's

Perspective article: the fate of collagen implants in tissue defects.

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The fate of collagen implants in a wound environment is determined by the host response they elicit, their accommodation for cellular infiltration and their susceptibility to proteolytic attack. Glutaraldehyde cross-linking is most effective in delaying resorption and reducing an antibody response.

Hormonal control of collagen metabolism. Part II.

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Natural and synthetic glucocorticoids are known to effect collagen metabolism. This influence is responsible for several side-effects of a long term therapy with glucocorticoids. Molecular mechanisms of these phenomena are complex, and are only partially elucidated. It has been found that

Collagen breakdown and ammonia inhalation.

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Measurement of several urinary metabolites of hydroxylysine indicates that considerable collagen degradation occurred in four individuals immediately after they had inhaled concentrated ammonia vapors. Since clinical and/or radiological evidence of intense upper respiratory and pulmonary

Distinct post-translational features of type I collagen are conserved in mouse and human periodontal ligament.

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OBJECTIVE Specifics of the biochemical pathways that modulate collagen cross-links in the periodontal ligament (PDL) are not fully defined. Better knowledge of the collagen post-translational modifications that give PDL its distinct tissue properties is needed to understand the pathogenic mechanisms

The activities of lysyl hydroxylase 3 (LH3) regulate the amount and oligomerization status of adiponectin.

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Lysyl hydroxylase 3 (LH3) has lysyl hydroxylase, galactosyltransferase, and glucosyltransferase activities, which are sequentially required for the formation of glucosylgalactosyl hydroxylysines in collagens. Here we demonstrate for the first time that LH3 also modifies the lysine residues in the

Downregulation of Glt25d1 aggravates carbon tetrachloride‑induced acute hepatic injury through activation of the TGF‑β1/Smad2 signaling pathway.

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Collagen β (1‑O) galactosyltransferase 1 (GLT25D1) has been reported to transfer galactose to hydroxylysine residues via β (1‑O) linkages in collagen. The present study investigated the function of the collagen galactosyltransferase activity of GLT25D1 against carbon tetrachloride (CCl4)‑induced

Peroxidasin forms sulfilimine chemical bonds using hypohalous acids in tissue genesis.

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Collagen IV comprises the predominant protein network of basement membranes, a specialized extracellular matrix, which underlie epithelia and endothelia. These networks assemble through oligomerization and covalent crosslinking to endow mechanical strength and shape cell behavior through

Metabolomics reveals elevated urinary excretion of collagen degradation and epithelial cell turnover products in irritable bowel syndrome patients.

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Irritable bowel syndrome (IBS), the most commonly diagnosed functional gastrointestinal (GI) disorder in developed countries, is characterized by chronic abdominal pain, and altered bowel habits.Accurate and timely diagnosis is challenging as it relies on

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