Mutual regulation between butyrate and hypoxia-inducible factor-1α in epithelial cell promotes expression of tight junction proteins.
Cell Biol Int
; 44(6): 1405-1414, 2020 Jun.
Article
en En
| MEDLINE
| ID: mdl-32129567
ABSTRACT
Inflammatory bowel disease is a kind of multi-aetiological chronic disease that is driven by multidimensional factors. Hypoxia-inducible factor-1α (HIF-1α) plays an important role in anti-inflammatory and cellular responses to hypoxia. Previous studies have found that B or T-cell-specific HIF-1α knock out mice exhibit severe colonic inflammation. However, we know very little about other functions of HIF-1α in intestinal epithelial cells (IECs). In our study, HIF-1αΔIEC mice were used to study the function of HIF-1α in IECs. HIF-1α was knocked down in Caco-2 cells by transfection with a small interfering (si) RNA. Immunohistochemical staining and western blotting were used to detect the expression of zonula occluden-1 (ZO-1) and Occludin. The content of colon was harvested for high-performance liquid chromatography analysis to examine the levels of butyrate in the gut. Our research found that HIF-1α played a protective role in dextran sulphate sodium-induced colitis, which was partly due to its regulation of tight junction (TJ) protein expression. Further study revealed that HIF-1α mediated TJ proteins levels by moderating the content of butyrate. Moreover, we found that butyrate regulated TJ protein expression, which is dependent on HIF-1α. These results indicated that there is a mutual regulatory mechanism between butyrate and HIF-1α, which has an important role in the maintenance of barrier function of the gastrointestinal tract.
Palabras clave
Texto completo:
1
Bases de datos:
MEDLINE
Asunto principal:
Butiratos
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Enfermedades Inflamatorias del Intestino
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Células Epiteliales
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Subunidad alfa del Factor 1 Inducible por Hipoxia
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Proteínas de Uniones Estrechas
Límite:
Animals
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Humans
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Male
Idioma:
En
Revista:
Cell Biol Int
Año:
2020
Tipo del documento:
Article
País de afiliación:
China