Imaging Inflammatory Hypoxia in the Murine Gut.
Methods Mol Biol
; 1422: 115-26, 2016.
Article
em En
| MEDLINE
| ID: mdl-27246027
ABSTRACT
The inflammatory bowel diseases (IBD), including Crohn's disease and ulcerative colitis, result in chronic inflammation to the gastrointestinal tract. In ulcerative colitis, inflammation tends to be more superficial and restricted to the colon; contrastingly, Crohn's disease presents as patchy, more penetrative inflammation that can occur throughout the gastrointestinal tract. Other differences between these diseases include the nature of their respective immune responses-Crohn's disease presents as a Th1 and ulcerative colitis as a Th2-type inflammation. During any inflammatory episode, metabolic demand on the tissue increases accompanying the influx of inflammatory cells, increasing the demand for ATP and oxygen. When availability of oxygen is limiting, tissues become hypoxic, which results in adaptive pathways to enable survival of hypoxic episodes. The primary pathway activated is the HIF (hypoxia inducible factor) transcription factor, which regulates adaptive pathways including genes controlling glycolytic metabolism and angiogenesis. In adequately oxygenated tissues (i.e. normoxia), the HIF protein is constantly produced, but oxygen-dependent enzymes called prolyl-hydroxylases utilize available oxygen to hydroxylate HIF on proline residues, targeting it for ubiquitination and subsequent degradation. Here we describe methods for inducing, visualizing, and quantifying in vivo "inflammatory hypoxia," using the murine gut as a model system.
Palavras-chave
Texto completo:
1
Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Doenças Inflamatórias Intestinais
/
Trato Gastrointestinal
Tipo de estudo:
Prognostic_studies
Limite:
Animals
Idioma:
En
Revista:
Methods Mol Biol
Ano de publicação:
2016
Tipo de documento:
Article