AI Article Synopsis

  • Inflammatory bowel disease (IBD) is linked to SUMOylation, a process involving post-translational modifications, with a focus on the role of deSUMOylases.
  • SENP7, a specific deSUMOylase, is found to be upregulated in intestinal epithelial cells during IBD, influencing inflammation and promoting the expansion of proinflammatory γδ T cells.
  • Knocking down SENP7 or depleting γδ T cells reduces gut inflammation, suggesting SENP7 as a crucial regulator in IBD and a promising target for therapeutic intervention.

Article Abstract

Inflammatory bowel disease (IBD) is a complex autoimmune disorder recently shown to be associated with SUMOylation, a post-translational modification mechanism. Here, we have identified a link between epithelial deSUMOylases and inflammation in IBD. DeSUMOylase SENP7 was seen to be upregulated specifically in intestinal epithelial cells in both human IBD and a mouse model. In steady state, but not IBD, SENP7 expression was negatively regulated by a direct interaction and ubiquitination by SIAH2. Upregulated SENP7 in inflamed tissue displayed a distinct interactome. These changes led to an expansion of localized proinflammatory γδ T cells. Furthermore, in vivo knockdown of SENP7 or depletion of γδ T cells abrogated dextran sulfate sodium (DSS)-induced gut inflammation. Strong statistical correlations between upregulated SENP7 and high clinical disease indices were observed in IBD patients. Overall, our data reveal that epithelial SENP7 is necessary and sufficient for controlling gut inflammation, thus highlighting its importance as a potential drug target.

Download full-text PDF

Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7617169PMC
http://dx.doi.org/10.1016/j.celrep.2019.11.028DOI Listing

Publication Analysis

Top Keywords

upregulated senp7
8
γδ t cells
8
gut inflammation
8
senp7
6
ibd
5
desumoylase senp7-mediated
4
epithelial
4
senp7-mediated epithelial
4
epithelial signaling
4
signaling triggers
4

Similar Publications

High glucose (HG), a hallmark of the tumour microenvironment, is also a biomechanical stressor, as it exerts hyper-osmotic stress (HG-HO), but not much is known regarding how tumour cells mechanoadapt to HG-HO. Therefore, this study aimed to delineate the novel molecular mechanisms by which tumour cells mechanoadapt to HG/HG-HO and whether phytochemical-based interference in these mechanisms can generate tumour-cell-selective vulnerability to cell death. Mannitol and L-glucose were used as hyper-osmotic equivalents of high glucose.

View Article and Find Full Text PDF

Disorganization of the basic contractile unit of muscle cells, i.e., the sarcomeres, leads to suboptimal force generation and is a hallmark of muscle atrophy.

View Article and Find Full Text PDF

Low-grade glioma (LGG) is an intracranial malignant tumour that mainly originates from astrocytes and oligodendrocytes. SUMOylation is one of the post-translational modifications but studies of SUMOylation in LGG is quite limited. Transcriptome data, single nucleotide variant (SNV) data and clinical data of LGG were derived from public databases.

View Article and Find Full Text PDF

Sarcoma-180 tumor affects the quality of oocytes in mice.

Oncol Lett

March 2021

The First Affiliated Hospital (School of Clinical Medicine), Guangdong Pharmaceutical University, Guangzhou, Guangdong 510080, P.R. China.

Numerous factors can affect the quality of oocytes; however, the effects of cancer on the quality of oocytes and the underlying mechanisms remain unclear. In the present study, the effects of the sarcoma-180 (S-180) cell line on the quality of oocytes were investigated using S-180 tumor-bearing mice. In total, 42 female C57BL/6J mice were randomly divided into the tumor-bearing group and the control group, with 21 mice per group.

View Article and Find Full Text PDF
Article Synopsis
  • Inflammatory bowel disease (IBD) is linked to SUMOylation, a process involving post-translational modifications, with a focus on the role of deSUMOylases.
  • SENP7, a specific deSUMOylase, is found to be upregulated in intestinal epithelial cells during IBD, influencing inflammation and promoting the expansion of proinflammatory γδ T cells.
  • Knocking down SENP7 or depleting γδ T cells reduces gut inflammation, suggesting SENP7 as a crucial regulator in IBD and a promising target for therapeutic intervention.
View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!