TY - JOUR
T1 - The pro-inflammatory cytokines IFNγ/TNFα increase chromogranin A-positive neuroendocrine cells in the colonic epithelium
AU - Hernández-Trejo, Antonio José
AU - Suárez-Pérez, Dimelza
AU - Gutiérrez-Martínez, Zenidel Itzel
AU - Fernandez-Vargas, Eduardo Omar
AU - Candelario-Martínez, Antonia Aurora
AU - Meraz-Ríos, Marco Antonio
AU - Citalán-Madrid, Alí Francisco
AU - Hernández-Ruíz, Marcela
AU - Reyes-Maldonado, Elba
AU - Valle-Rios, Ricardo
AU - Feintuch-Unger, Jacobo H.
AU - Villegas-Sepúlveda, Nicolás
AU - Medina-Contreras, Oscar
AU - Serrano, Carolina
AU - Michael, Schnoor
AU - Nava, Porfirio
N1 - Publisher Copyright:
© 2016 The Author(s); published by Portland Press Limited on behalf of the Biochemical Society.
PY - 2016
Y1 - 2016
N2 - The 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.
AB - The 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.
UR - http://www.scopus.com/inward/record.url?scp=85009454706&partnerID=8YFLogxK
U2 - 10.1042/BCJ20160390
DO - 10.1042/BCJ20160390
M3 - Artículo
SN - 0264-6021
VL - 473
SP - 3805
EP - 3818
JO - Biochemical Journal
JF - Biochemical Journal
IS - 21
ER -