Published online Feb 21, 2019. doi: 10.3748/wjg.v25.i7.824
Peer-review started: November 12, 2018
First decision: November 29, 2018
Revised: January 10, 2019
Accepted: January 18, 2019
Article in press: January 18, 2019
Published online: February 21, 2019
Processing time: 108 Days and 1.6 Hours
Ubiquitin-specific protease 22 (USP22) is a novel member of the USPs subfamily, acting as a regulator of cell cycle progression, proliferation, and tumor invasion. Decreased expression of USP22 has been identified to contribute to arrested cell cycle and disrupted generation of differentiated cell types in crypts and villi. However, the regulatory mechanism of USP22 remains unclear. Therefore, elucidation of the underlying mechanism may help to improve the tissue repair in intestinal ischemia reperfusion (I/R) injury.
It is necessary to explore whether USP22 is correlated with increased potential of cell proliferation and tissue regeneration in intestinal I/R injury. Recent studies have demonstrated that insufficient proliferation and regeneration of fully rescuing intestinal mucosal barrier function could be witnessed by the high mortality rate in clinical practice. Moreover, the potential role of USP22 in cell growth, cell cycle progression, and generation of differentiated cell types has also been reported in crypts and villi. These findings give us a good lead for further study regarding the mechanism of USP22 regulation during intestinal I/R injury.
In the previous study, we investigated the effect of USP22 on intestinal cell proliferation and regeneration after intestinal I/R injury both in vivo and in vitro by gain- and loss-of-function approaches. Our study provides significant insight into the signalling mechanism of USP22 during intestinal I/R injury that may contribute to the future investigation of more effective therapies in clinical practice.
Experiments using an animal model and in vitro model in rats and cells to better elucidate the pathophysiological process of intestinal I/R injury. Hematoxylin and eosin staining and Chiu’s scoring system were used to demonstrate the intestinal tissue injury histopathologically. Immunohistochemical staining for PCNA was carried out to display and observe positive nuclei of proliferating intestinal cells. Gene silencing or transfection was conducted to construct relatively stable USP22-depleted or -expressed cells to complete the following functional studies. A series of in vitro experiments, such as Western blot, Cell Counting Kit-8, and cell cycle analysis, were performed to explore the effect of USP22 on cell proliferation.
Experiments in vivo showed the correlation between USP22 and intestinal regenerative activity of intestinal cells after intestinal I/R injury. The results of in vitro experiments showed a direct positive correlation of USP22 with cell proliferation and cell cycle progression of intestinal cells after hypoxia/reoxygenation injury. This study could be valuable for consultation in further study on intestinal I/R injury and be potentially utilized in therapeutic enhancement in clinical practice. Limitations did exist that the in vivo study should be better designed to imply causation and biological linkage and USP22 knockout mouse models would be helpful. Clinical samples are also needed to better suit the application on human beings.
USP22 plays a positive role in intestinal epithelial cell proliferation and tissue regeneration in intestinal I/R injury. This study reveals a novel role for USP22 in intestinal regeneration after I/R injury. Targeting USP22 may increase the therapeutic potential for intestinal I/R injury in clinical practice.
Our study illuminates the role of USP22 in intestinal epithelial cell proliferation and tissue regeneration in intestinal I/R injury. Other researchers have reported the abundant mucus secreting goblet cells in a USP22 globally reduced mouse model. While goblet cells are also one of indispensable parts in regulating innate immune function, further investigation is needed.