Abstract
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. 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. NoxO1 affects colon epithelium homeostasis and prevents inflammation.
Highlights
Colon is an organ with an enormous tissue turnover, i.e., a relatively high level of cell renewal
The predominant isoforms found in the intestinal system are Nox1 and Duox2, with Nox1 being mainly expressed in the ileum, cecum, and colon, while Duox2 can be found in all compartments of the intestinal tract [7]
NoxO1 Is Highly Expressed in the Colon Epithelium
Summary
Colon is an organ with an enormous tissue turnover, i.e., a relatively high level of cell renewal. The predominant isoforms found in the intestinal system are Nox and Duox, with Nox being mainly expressed in the ileum, cecum, and colon, while Duox can be found in all compartments of the intestinal tract [7] Both Nox and Duox have been shown to play a role in the development, progression, NoxO1 Controls Colon Cell Proliferation and healing of ulcerative colitis [8,9,10,11]. In human colon cancer cells, proteasomal degradation of NoxO1 reduces the Nox1-dependent ROS formation, and expression and stability of NoxO1 were significantly increased in human colon cancer tissues compared to normal colon [18]. This finding suggests a role of NoxO1 in cancer. This includes NoxO1s localization and its role in the production of ROS in the colon
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
