nasal polyps/hypoxie

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The effect of hypoxia and cycloxygenase inhibitors on nasal polyp derived fibroblasts.

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OBJECTIVE The pathogenesis of chronic rhinosinusitis with nasal polyposis is unknown. Chronic inflammation along with local tissue hypoxia may effect polyp's growth. Activation of Cycloxygenases may also be involved. COX-2 up-regulates in response to different stimuli including hypoxia. Its

[Expression of hypoxia-inducible factor-1alpha in nasal polyps and its correlation with vascular endothelial growth factor and inducible nitric oxide synthase].

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OBJECTIVE To detect the expression and distribution of hypoxia-inducible factor-1alpha (HIF-1alpha) in nasal polyps, to explore the relationship of HIF-1alpha with vascular endothelial growth factor (VEGF) and inducible nitric oxide synthase (iNOS), and to investigate the role of HIF-1alpha in the

Hypoxia regulates IL-17A secretion from nasal polyp epithelial cells.

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Hypoxia creates a microenvironment conducive to polypogenesis by regulating immune responses of the nasal polyp (NP) epithelium. We explored the immunocompetence of NP and control epithelial cells in response to hypoxia, to investigate potential relationships with polypogenesis. Three groups of

[Hypoxia effects on vascular endothelial growth factor derived epithelial cells of nasal polyps].

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OBJECTIVE To understand the role of nasal mucous epithelial cells to hypoxia in early stage of nasal polyps(NP) formation. METHODS Epithelial cells of NP and inferior turbinate (IT) were cultured without serum under normal oxygen and hypoxia, and stimulus of inflammatory cytokines. Erythropoietin

Expression of hypoxia-inducible factor 1alpha in the nasal polyps by real-time RT-PCR and immunohistochemistry.

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OBJECTIVE Hypoxia may result in increased recruitment of inflammatory cells and release of various inflammatory cytokines. Local hypoxia within the sinus is believed to aggravate sinus inflammation. In this study, we tried to investigate the correlation of hypoxia-inducible factor, which is

Hypoxia stimulates inflammatory and fibrotic responses from nasal-polyp derived fibroblasts.

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OBJECTIVE Chronic sinusitis is primarily an inflammatory disorder characterized by hyperplasia of immune cells and sinus tissue. Nasal mucosal swelling or polyps can occlude the sinus ostia, decreasing the level of oxygen available to the sinus tissue. Hypoxia in many diseases results in increased

Overexpression of hypoxia-inducible factor 1α is associated with neutrophilic inflammation in chronic rhinosinusitis with nasal polyps.

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This study aimed to assess the possible role of hypoxia-inducible factor 1α (HIF-1α) in promoting neutrophilic inflammation in chronic rhinosinusitis with nasal polyps (CRSwNP) patients.We examined HIF-1α expression in sinonasal tissues from CRSwNP patients

Hypoxia induces cysteine-rich 61, vascular endothelial growth factor, and interleukin-8 expressions in human nasal polyp fibroblasts: An implication of neutrophils in the pathogenesis of nasal polyposis.

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BACKGROUND The purpose of this article was to elucidate the roles of neutrophils and angiogenesis factors in the pathogenesis of nasal polyposis. The effect of hypoxia on the expressions of angiogenesis factors as cysteine-rich 61 (Cyr61) and vascular endothelial growth factor (VEGF) and neutrophil

Hypoxia-stimulated vascular endothelial growth factor production in human nasal polyp fibroblasts: effect of epigallocatechin-3-gallate on hypoxia-inducible factor-1 alpha synthesis.

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OBJECTIVE To verify the inhibitory effects of epigallocatechin-3-gallate (EGCG) on the synthesis of hypoxia-induced vascular endothelial growth factor (VEGF) in nasal polyp fibroblasts (NPFs). METHODS Eight primary cultures of NPFs were established from nasal polyps. Effects of EGCG on the

Increased expression of hypoxia-inducible factor 1alpha in the nasal polyps.

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OBJECTIVE The etiology and mechanism of nasal polyps are still not well known. A newly discovered transcriptional factor, hypoxia-inducible factor (HIF), is a DNA-binding protein. Hypoxia-inducible factor is demonstrated to associate with various neoplasms. We investigate the expression of

Nox4 mediates hypoxia-stimulated myofibroblast differentiation in nasal polyp-derived fibroblasts.

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BACKGROUND Chronic hypoxia is associated with remodeling in various organs. Reactive oxygen species (ROS) derived from NADPH oxidases (Nox), and transforming growth factor-β(1) (TGF-β(1)) have been implicated in the pathogenesis of hypoxia-induced remodeling. The aims of this study were to determine

Local tissue hypoxia and formation of nasal polyps.

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OBJECTIVE To explore the response of nasal mucosa epithelial cells to hypoxia in terms of formation of nasal polyps (NP). METHODS Epithelial cells of NP and inferior turbinate (IT) were cultured serum-free under normal oxygen and hypoxic circumstances with stimulation of IL-1 beta and TNF alpha. The

Sirtuin 6 modulates hypoxia-induced autophagy in nasal polyp fibroblasts via inhibition of glycolysis.

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BACKGROUND To elucidate the interaction between hypoxia-induced autophagy and glycolysis in nasal polyp fibroblasts, and the regulatory role of Sirtuin 6 (SIRT6) in the pathogenesis of nasal polyp. OBJECTIVE Through examining the expressions of lactate dehydrogenase (LDH), microtubule-associated

Vγ1⁺ γδT Cells Are Correlated With Increasing Expression of Eosinophil Cationic Protein and Metalloproteinase-7 in Chronic Rhinosinusitis With Nasal Polyps Inducing the Formation of Edema.

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OBJECTIVE We have found that expression of γδT cells is increased in pathological mucosa of chronic rhinosinusitis with nasal polyps (CRSwNP) compared with normal nasal mucosa. This increase is correlated with the infiltration of eosinophils in CRSwNP. Here, we investigated the expression of γδT

Role of hypoxia-inducible factor-1α expression in regulatory T cells on nasal polypogenesis.

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OBJECTIVE Hypoxia-inducible factor-1α (HIF-1α) is considered as a key molecule in regulating Th17:regulatory T-cells (Tregs) balance. The aims of this study were to investigate whether HIF-1α is associated with the RORγ (RAR-related orphan receptor gamma) expression of Tregs in nasal polyps and to

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