TY  - JOUR
A1  - Moll, Franziska
A1  - Walter, Maria
A1  - Rezende Felipe, Flávia Figueiredo de
A1  - Helfinger, Valeska
A1  - Vasconez, Andrea Estefania
A1  - Oliveira, Tiago de
A1  - Greten, Florian
A1  - Olesch, Catherine
A1  - Weigert, Andreas
A1  - Radeke, Heinfried H.
A1  - Schröder, Katrin
T1  - NoxO1 controls proliferation of colon epithelial cells
T2  - Frontiers in immunology
N2  - Aim: Reactive oxygen species (ROS) produced by enzymes of the NADPH oxidase family serve as second messengers for cellular signaling. Processes such as differentiation and proliferation are regulated by NADPH oxidases. In the intestine, due to the exceedingly fast and constant renewal of the epithelium both processes have to be highly controlled and balanced. Nox1 is the major NADPH oxidase expressed in the gut, and its function is regulated by cytosolic subunits such as NoxO1. We hypothesize that the NoxO1-controlled activity of Nox1 contributes to a proper epithelial homeostasis and renewal in the gut.
Results: NoxO1 is highly expressed in the colon. Knockout of NoxO1 reduces the production of superoxide in colon crypts and is not subsidized by an elevated expression of its homolog p47phox. Knockout of NoxO1 increases the proliferative capacity and prevents apoptosis of colon epithelial cells. In mouse models of dextran sulfate sodium (DSS)-induced colitis and azoxymethane/DSS induced colon cancer, NoxO1 has a protective role and may influence the population of natural killer cells.
Conclusion: NoxO1 affects colon epithelium homeostasis and prevents inflammation.
KW  - reactive oxygen species
KW  - colon
KW  - Nox1
KW  - NoxO1
KW  - proliferation
KW  - inflammation
Y1  - 2018
UR  - http://publikationen.ub.uni-frankfurt.de/frontdoor/index/index/docId/50155
UR  - https://nbn-resolving.org/urn:nbn:de:hebis:30:3-501559
SN  - 1664-3224
N1  - Copyright: © 2018 Moll, Walter, Rezende, Helfinger, Vasconez, De Oliveira, Greten, Olesch, Weigert, Radeke and Schröder. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
VL  - 9
IS  - Art. 973
SP  - 1
EP  - 11
PB  - Frontiers Media
CY  - Lausanne
ER  -