colitis/hypoxia

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Role of hypoxia-inducible factor-1α in pathogenesis and disease evaluation of ulcerative colitis.

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The main aim of the present study was to measure hypoxia-inducible factor-1α (HIF-1α) in serum and colonic mucosa of ulcerative colitis (UC) patients and to analyze its role in the pathogenesis, disease activity and severity of UC. A total of 47 UC patients and 13 UC in remission patients were

Hypoxia-inducible factor 1 alpha and vascular endothelial growth factor overexpression in ischemic colitis.

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OBJECTIVE To examine the etiology and pathophysiology in human ischemic colitis from the viewpoint of ischemic factors such as hypoxia-inducible factor 1 alpha (HIF-1 alpha and vascular endothelial growth factor (VEGF). METHODS Thirteen patients with ischemic colitis and 21 normal controls underwent

Relationship between inflammation and tissue hypoxia in a mouse model of chronic colitis.

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BACKGROUND Hypoxia has been reported to be associated with the colonic inflammation observed in a chemically induced mouse model of self-limiting colitis, suggesting that low tissue oxygen tension may play a role in the pathophysiology of inflammatory tissue injury. However, no studies have been

Myeloid Cell Hypoxia-Inducible Factors Promote Resolution of Inflammation in Experimental Colitis.

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Colonic tissues in Inflammatory Bowel Disease (IBD) patients exhibit oxygen deprivation and activation of hypoxia-inducible factor 1α and 2α (HIF-1α and HIF-2α), which mediate cellular adaptation to hypoxic stress. Notably, macrophages and neutrophils accumulate preferentially in hypoxic regions of

Knockdown of myeloid cell hypoxia-inducible factor-1α ameliorates the acute pathology in DSS-induced colitis.

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Inflammation and hypoxia are hallmarks of inflammatory bowel disease. Low oxygen levels activate hypoxia-inducible factors as central transcriptional regulators of cellular responses to hypoxia, particularly in myeloid cells where hypoxia-inducible factors control immune cell function and survival.

[Effect of acupuncture and moxibustion on expression of signal transducers and activators of transcription 3 and hypoxia-inducible factor 1α in colon mucosa in ulcerative colitis mice]

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Objective: To investigate the effect of acupuncture or moxibustion of "Zusanli" (ST36) and "Guanyuan" (CV4) on expression of signal transducers and activators of transcription 3 (STAT3) and hypoxia-inducible factor 1α (HIF-1α) in colonic

Intrarectal administration of oxygenated perfluorodecalin promotes healing of murine colitis by targeting inflammatory hypoxia.

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Intestinal inflammation is associated with enhanced mucosal hypoxia, which contributes to the ongoing inflammatory process and hampers appropriate mucosal healing. We questioned whether local treatment with an oxygen (O(2))-carrying and -releasing molecule (oxygenated perfluorodecalin, O(2)-PFD)

Therapeutic treatment with a novel hypoxia-inducible factor hydroxylase inhibitor (TRC160334) ameliorates murine colitis.

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OBJECTIVE Mucosal healing in inflammatory bowel disease (IBD) can be achieved by improvement of intestinal barrier protection. Activation of hypoxia-inducible factor (HIF) has been identified as a critical factor for barrier protection during mucosal insult and is linked with improvement in symptoms

Inverse correlation between metallothioneins and hypoxia-inducible factor 1 alpha in colonocytes and experimental colitis.

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A positive-feedback mechanism between hypoxia-inducible factor 1 alpha (HIF-1α) and metallothioneins (MTs) has been identified in different diseases. Both proteins have been independently proposed in the pathogenesis of inflammatory bowel disease (IBD); however, their relation has never been studied

Temporal induction of intestinal epithelial hypoxia-inducible factor-2α is sufficient to drive colitis.

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Hypoxia is a notable feature of inflammatory bowel disease and chronic induction of hypoxia-inducible factor (HIF)-1α and HIF-2α (endothelial PAS domain protein 1, EPAS1) play important, but opposing, roles in its pathogenesis. While activation of HIF-1α decreases intestinal inflammation and is

Markers of Hypoxia Correlate with Histologic and Endoscopic Severity of Colitis in Inflammatory Bowel Disease.

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Inflammation results in significant shifts in tissue metabolism. Recent studies indicate that inflammation and hypoxia occur concomitantly. We examined whether circulating and tissue markers of hypoxia could serve as surrogate indicators of disease severity in adult and pediatric

Hypoxia-inducible factor 1 in dendritic cells is crucial for the activation of protective regulatory T cells in murine colitis.

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Dendritic cells (DCs) serve as a bridge between innate and adaptive immunity and help to maintain intestinal homeostasis. Inflammatory bowel disease (IBD) is associated with dysregulation of the mucosal immune response. The concomitant hypoxic inflammation in IBD will activate the transcription

Epithelial hypoxia-inducible factor-1 is protective in murine experimental colitis.

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Mucosal epithelial cells are uniquely equipped to maintain barrier function even under adverse conditions. Previous studies have implicated hypoxia in mucosal tissue damage resulting from both acute and chronic inflammation. Given the importance of the transcriptional regulator hypoxia-inducible

Proresolution effects of hydrogen sulfide during colitis are mediated through hypoxia-inducible factor-1α.

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During a course of colitis, production of the gaseous mediator hydrogen sulfide (H2S) is markedly up-regulated at sites of mucosal damage and contributes significantly to healing and resolution of inflammation. The signaling mechanisms through which H2S promotes resolution of colitis are unknown. We

Hypoxia-inducible factor augments experimental colitis through an MIF-dependent inflammatory signaling cascade.

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OBJECTIVE Colon epithelial cells are critical for barrier function and contain a highly developed immune response. A previous study has shown hypoxia-inducible factor (HIF) as a critical regulator of barrier protection during colon epithelial injury. However, the role of HIF signaling in colon

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