The pro-inflammatory cytokines IFNγ/TNFα increase chromogranin A-positive neuroendocrine cells in the colonic epithelium
2016; Portland Press; Volume: 473; Issue: 21 Linguagem: Inglês
10.1042/bcj20160390
ISSN1470-8728
AutoresJosé Antonio Hernández-Trejo, Dimelza Suárez-Pérez, Itzel Zenidel Gutiérrez-Martínez, Omar Vargas, Carolina Serrano, Aurora Candelario‐Martínez, Marco Antonio Meraz‐Ríos, Alí Francisco Citalán‐Madrid, Marcela Hernández-Ruíz, Elba Reyes‐Maldonado, Ricardo Valle-Ríos, Jacobo H. Feintuch-Unger, Michael Schnoor, Nicolás Villegas‐Sepúlveda, Óscar Medina‐Contreras, Porfirio Nava,
Tópico(s)Pancreatic function and diabetes
ResumoThe gastrointestinal tract is the largest hormone-producing organ in the body due to a specialized cell population called enteroendocrine cells (EECs). The number of EECs increases in the mucosa of inflammatory bowel disease patients; however, the mechanisms responsible for these changes remain unknown. Here, we show that the pro-inflammatory cytokines interferon γ (IFNγ) and tumor necrosis factor α (TNFα) or dextran sulfate sodium (DSS)-induced colitis increase the number of EECs producing chromogranin A (CgA) in the colonic mucosa of C57BL/6J mice. CgA-positive cells were non-proliferating cells enriched with inactive phosphatase and tensin homolog deleted on chromosome 10 (PTEN) and autophagy markers. Moreover, inhibition of Akt and autophagy prevented the increase in CgA-positive cells after IFNγ/TNFα treatment. Similarly, we observed that CgA-positive cells in the colonic mucosa of patients with colitis expressed Akt and autophagy markers. These findings suggest that Akt signaling and autophagy control differentiation of the intestinal EEC lineage during inflammation.
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