gelatinase/hypoxia

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Neutrophil gelatinase-associated lipocalin: its response to hypoxia and association with acute mountain sickness.

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Acute Mountain Sickness (AMS) is a common clinical challenge at high altitude (HA). A point-of-care biochemical marker for AMS could have widespread utility. Neutrophil gelatinase-associated lipocalin (NGAL) rises in response to renal injury, inflammation and oxidative stress. We investigated

Hypoxia augments gelatinase activity in a variety of adenocarcinomas in vitro.

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BACKGROUND Hypoxia within solid adenocarcinomas and protease up-regulation has been independently implicated as poor prognostic indicators in a variety of tumor types. The authors hypothesize that Matrix Metalloproteases (MMP) are up-regulated in direct response to a hypoxic

Hypoxia-ischemia or excitotoxin-induced tissue plasminogen activator- dependent gelatinase activation in mice neonate brain microvessels.

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Hypoxia-ischemia (HI) and excitotoxicity are validated causes of neonatal brain injuries and tissue plasminogen activator (t-PA) participates in the processes through proteolytic and receptor-mediated pathways. Brain microvascular endothelial cells from neonates in culture, contain and release more

Neutrophil gelatinase-associated lipocalin protects renal tubular epithelial cells in hypoxia-reperfusion by reducing apoptosis.

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OBJECTIVE The aim of this study was to elucidate the role of neutrophil gelatinase-associated lipocalin (NGAL) in regulating apoptosis of tubular epithelial cells in a hypoxia-reperfusion model. METHODS A hypoxia-reperfusion model was established with NRK-52E cells to assess apoptosis and cell cycle

[Protective effect and mechanism of neutrophil gelatinase-associated lipocalin against hypoxia/reoxygenation injury of HK-2 renal tubular epithelial cells].

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Objective To study the role of neutrophil gelatinase-associated lipocalin (NGAL) in hypoxia/reoxygenation injury and its regulatory effect on autophagy in HK-2 renal tubular epithelial cells. Methods Three sets of designed NGAL short-hairpin RNA (shRNA) sequences were synthesized and transfected

Inhibition of gelatinase activity reduces neural injury in an ex vivo model of hypoxia-ischemia.

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Perinatal hypoxia-ischemia (H-I) often manifests as cognitive and/or motor disturbances that appear early in development. Growing evidence indicates that neuroinflammation may exacerbate H-I injury. Resident microglia release proinflammatory cytokines and proteases in response to ischemia. Matrix

Hypoxia Stimulates Synthesis of Neutrophil Gelatinase-Associated Lipocalin in Aortic Valve Disease.

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Objective: Aortic valve disease is commonly found in the elderly population. It is characterized by dysregulated extracellular matrix remodeling followed by extensive microcalcification of the aortic valve and activation of valve interstitial cells. The mechanism behind these events are

Protective effects of neutrophil gelatinase-associated lipocalin on hypoxia/reoxygenation injury of HK-2 cells.

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BACKGROUND Neutrophil gelatinase-associated lipocalin (NAGL) was first extracted from neutrophil granules. Our previous study showed that the expression of NGAL mRNA and protein can be induced by hypoxia/reoxygenation. This study was designed to investigate the relationship between NGAL and

Association between plasma neutrophil gelatinase associated lipocalin level and obstructive sleep apnea or nocturnal intermittent hypoxia.

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BACKGROUND Both obstructive sleep apnea (OSA) and a novel lipocalin, neutrophil gelatinase associated lipocalin (Ngal), have been reported to be closely linked with cardiovascular disease and loss of kidney function through chronic inflammation. However, the relationship between OSA and Ngal has

Neutrophil Gelatinase-Associated Lipocalin2 Exaggerates Cardiomyocyte Hypoxia Injury by Inhibiting Integrin β3 Signaling.

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BACKGROUND The neutrophil inflammatory protein, lipocalin-2 (NGAL), is elevated in certain forms of cardiac hypertrophy and acute heart failure. However, the specific role of NGAL in cardiac hypoxia injury is unclear. This study aimed to elucidate the functional role of NGAL in cardiomyocyte hypoxia

Chitosan-shelled oxygen-loaded nanodroplets abrogate hypoxia dysregulation of human keratinocyte gelatinases and inhibitors: New insights for chronic wound healing.

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BACKGROUND In chronic wounds, efficient epithelial tissue repair is hampered by hypoxia, and balances between the molecules involved in matrix turn-over such as matrix metalloproteinases (MMPs) and tissue inhibitors of metalloproteinases (TIMPs) are seriously impaired. Intriguingly, new oxygenating

Gelatinase expression in pulmonary arteries during experimental pulmonary hypertension.

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Structural remodelling of pulmonary vessels is an important feature of pulmonary hypertension (PH), which reflects distal artery muscularization and matrix remodelling. The matrix metalloproteinases (MMPs) are involved in extracellular matrix turnover and hence, in smooth muscle cell migration and

Hypoxia upregulates angiogenesis and synovial cell migration in rheumatoid arthritis.

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BACKGROUND Rheumatoid arthritis (RA) is characterised by invasion of cartilage, bone and tendon by inflamed synovium. Previous studies in our laboratory have shown that hypoxia is a feature of RA synovitis. In the present study, we investigated the consequences of hypoxia on angiogenesis and

Pulmonary interstitial pressure and tissue matrix structure in acute hypoxia.

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Pulmonary interstitial pressure was measured via micropuncture in anesthetized rabbits in normoxia and after breathing 12% O(2). In normoxia [arterial PO(2) = 88 +/- 2 (SD) mmHg], pulmonary arterial pressure and pulmonary interstitial pressure were 16 +/- 8 and -9.6 +/- 2 cmH(2)O, respectively.

Studies of type IV collagenase regulation by hypoxia.

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Recent data suggest that patients with more hypoxic solid tumors are more likely to develop metastases and die. We speculated that upregulation of the metastasis-associated type IV collagenase MMP-9 (gelatinase B) by hypoxia might be correlated with the increased risk of distant failure in patients

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