The Role of Keratins in Epithelial Homeostasis

Skin Barrier ◽  
2005 ◽  
pp. 161-190
Keyword(s):  
Epithelial Homeostasis

The Role of Serotonin in Intestinal Epithelial Homeostasis

2010 ◽  
Vol 158 (2) ◽  
pp. 186
Author(s):  
E.R. Gross ◽  
A.R. Ruiz-Elizalde ◽  
Z.V. Gertsberg ◽  
M.D. Gershon ◽  
R.A. Cowles
Keyword(s):  
Intestinal Epithelial ◽  
Epithelial Homeostasis

scholarly journals Loss of intestinalO-glycans promotes spontaneous duodenal tumors

2016 ◽  
Vol 311 (1) ◽  
pp. G74-G83 ◽  
Author(s):  
Nan Gao ◽  
Kirk Bergstrom ◽  
Jianxin Fu ◽  
Biao Xie ◽  
Weichang Chen ◽  
...  
Keyword(s):  
Small Intestine ◽  
Inflammatory Responses ◽  
Tumor Development ◽  
Duodenal Mucosa ◽  
Intestinal Epithelial ◽  
Double Knockout ◽  
Adult Mice ◽  
Epithelial Homeostasis ◽  
Mucus Barrier

Mucin-type O-glycans, primarily core 1- and core 3-derived O-glycans, are the major mucus barrier components throughout the gastrointestinal tract. Previous reports identified the biological role of O-glycans in the stomach and colon. However, the biological function of O-glycans in the small intestine remains unknown. Using mice lacking intestinal core 1- and core 3-derived O-glycans [intestinal epithelial cell C1galt1−/−; C3GnT−/−or double knockout (DKO)], we found that loss of O-glycans predisposes DKO mice to spontaneous duodenal tumorigenesis by ∼1 yr of age. Tumor incidence did not increase with age; however, tumors advanced in aggressiveness by 20 mo. O-glycan deficiency was associated with reduced luminal mucus in DKO mice before tumor development. Altered intestinal epithelial homeostasis with enhanced baseline crypt proliferation characterizes these phenotypes as assayed by Ki67 staining. In addition, fluorescence in situ hybridization analysis reveals a significantly lower bacterial burden in the duodenum compared with the large intestine. This phenotype is not reduced with antibiotic treatment, implying O-glycosylation defects, rather than bacterial-induced inflammation, which causes spontaneous duodenal tumorigenesis. Moreover, inflammatory responses in DKO duodenal mucosa are mild as assayed with histology, quantitative PCR for inflammation-associated cytokines, and immunostaining for immune cells. Importantly, inducible deletion of intestinal O-glycans in adult mice leads to analogous spontaneous duodenal tumors, although with higher incidence and heightened severity compared with mice with O-glycans constitutive deletion. In conclusion, these studies reveal O-glycans within the small intestine are critical determinants of duodenal cancer risk. Future studies will provide insights into the pathogenesis in the general population and those at risk for this rare but deadly cancer.

scholarly journals The role of IL-22 in intestinal health and disease

2020 ◽  
Vol 217 (3) ◽  
Author(s):  
Mary E. Keir ◽  
Tangsheng Yi ◽  
Timothy T. Lu ◽  
Nico Ghilardi
Keyword(s):  
Host Defense ◽  
Epithelial Barrier ◽  
Antimicrobial Proteins ◽  
Epithelial Barrier Function ◽  
Graft Versus Host ◽  
Interleukin 22 ◽  
Epithelial Homeostasis ◽  
Health And Disease ◽  
Inflammatory Bowel

The cytokine interleukin-22 (IL-22) is a critical regulator of epithelial homeostasis. It has been implicated in multiple aspects of epithelial barrier function, including regulation of epithelial cell growth and permeability, production of mucus and antimicrobial proteins (AMPs), and complement production. In this review, we focus specifically on the role of IL-22 in the intestinal epithelium. We summarize recent advances in our understanding of how IL-22 regulates homeostasis and host defense, and we discuss the IL-22 pathway as a therapeutic target in diseases of the intestine, including inflammatory bowel disease (IBD), graft-versus-host disease (GVHD), and cancer.

Role of Oxygen in Corneal Epithelial Homeostasis During Extended Contact Lens Wear

2003 ◽  
pp. S2-S6 ◽  
Author(s):  
Patrick M. Ladage ◽  
James V. Jester ◽  
W. Matthew Petroll ◽  
Jan P.G. Bergmanson ◽  
H. Dwight Cavanagh
Keyword(s):  
Contact Lens ◽  
Corneal Epithelial ◽  
Contact Lens Wear ◽  
Epithelial Homeostasis ◽  
Extended Contact ◽  
Lens Wear

scholarly journals Cytoplasmic pressure maintains epithelial integrity and inhibits cell motility

2021 ◽  
Author(s):  
Pragati Chengappa ◽  
Tia M Jones ◽  
James M Cowan ◽  
Devneet Kaur Kainth ◽  
Ryan J Petrie
Keyword(s):  
Epithelial To Mesenchymal Transition ◽  
Three Dimensional ◽  
Response To Treatment ◽  
Epithelial Tissue ◽  
Mesenchymal Transition ◽  
Tissue Integrity ◽  
Epithelial Homeostasis ◽  
Cell Protrusion ◽  
Lamellipodia Formation

Cytoplasmic pressure, a function of actomyosin contractility and water flow, can regulate cellular morphology and dynamics. In mesenchymal cells, cytoplasmic pressure powers cell protrusion through physiological three-dimensional extracellular matrices. However, the role of intracellular pressure in epithelial cells is relatively unclear. Here we find that high cytoplasmic pressure is necessary to maintain barrier function, one of the hallmarks of epithelial homeostasis. Further, our data show that decreased cytoplasmic pressure facilitates lamellipodia formation during the epithelial to mesenchymal transition (EMT). Critically, activation of the actin nucleating protein Arp2/3 is required for the reduction in cytoplasmic pressure and lamellipodia formation in response to treatment with hepatocyte growth factor (HGF) to induce EMT. Thus, elevated cytoplasmic pressure functions to maintain epithelial tissue integrity, while reduced cytoplasmic pressure triggers lamellipodia formation and motility during HGF-dependent EMT.

scholarly journals P19 The Role Of Differential Tnfr Signalling In Maintenance Of Alveolar Epithelial Homeostasis

Thorax ◽  
2014 ◽  
Vol 69 (Suppl 2) ◽  
pp. A85-A86
Author(s):  
F. Millar ◽  
A. Proudfoot ◽  
D. Salman ◽  
C. Summers ◽  
P. Morley ◽  
...  
Keyword(s):  
Alveolar Epithelial ◽  
Epithelial Homeostasis

scholarly journals SETDB1 is required for intestinal epithelial differentiation and the prevention of intestinal inflammation

Gut ◽  
2020 ◽  
pp. gutjnl-2020-321339 ◽  
Author(s):  
Lea Južnić ◽  
Kenneth Peuker ◽  
Anne Strigli ◽  
Mario Brosch ◽  
Alexander Herrmann ◽  
...  
Keyword(s):  
Rare Variants ◽  
Intestinal Inflammation ◽  
Specific Activity ◽  
Critical Role ◽  
Epithelial Differentiation ◽  
Endogenous Retroviruses ◽  
Intestinal Epithelial ◽  
Loss Of Function ◽  
Epithelial Homeostasis

ObjectiveThe intestinal epithelium is a rapidly renewing tissue which plays central roles in nutrient uptake, barrier function and the prevention of intestinal inflammation. Control of epithelial differentiation is essential to these processes and is dependent on cell type-specific activity of transcription factors which bind to accessible chromatin. Here, we studied the role of SET Domain Bifurcated Histone Lysine Methyltransferase 1, also known as ESET (SETDB1), a histone H3K9 methyltransferase, in intestinal epithelial homeostasis and IBD.DesignWe investigated mice with constitutive and inducible intestinal epithelial deletion of Setdb1, studied the expression of SETDB1 in patients with IBD and mouse models of IBD, and investigated the abundance of SETDB1 variants in healthy individuals and patients with IBD.ResultsDeletion of intestinal epithelial Setdb1 in mice was associated with defects in intestinal epithelial differentiation, barrier disruption, inflammation and mortality. Mechanistic studies showed that loss of SETDB1 leads to de-silencing of endogenous retroviruses, DNA damage and intestinal epithelial cell death. Predicted loss-of-function variants in human SETDB1 were considerably less frequently observed than expected, consistent with a critical role of SETDB1 in human biology. While the vast majority of patients with IBD showed unimpaired mucosal SETDB1 expression, comparison of IBD and non-IBD exomes revealed over-representation of individual rare missense variants in SETDB1 in IBD, some of which are predicted to be associated with loss of function and may contribute to the pathogenesis of intestinal inflammation.ConclusionSETDB1 plays an essential role in intestinal epithelial homeostasis. Future work is required to investigate whether rare variants in SETDB1 contribute to the pathogenesis of IBD.

Role of 14-3-3ζ Signaling in the Regulation of Intestinal Epithelial Homeostasis

2014 ◽  
Vol 186 (2) ◽  
pp. 679
Author(s):  
N. Hansraj ◽  
J.N. Rao ◽  
D.J. Turner ◽  
J. Wang
Keyword(s):  
Intestinal Epithelial ◽  
Epithelial Homeostasis

scholarly journals Prognostic Role of Inflammasome Components in Human Colorectal Cancer

Cancers ◽  
2020 ◽  
Vol 12 (12) ◽  
pp. 3500
Author(s):  
Charlotte Domblides ◽  
Isabelle Soubeyran ◽  
Lydia Lartigue ◽  
Isabelle Mahouche ◽  
Félix Lefort ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Survival Rates ◽  
Death Receptor ◽  
Immunofluorescence Assay ◽  
Prognostic Impact ◽  
Human Colorectal Cancer ◽  
Entire Cohort ◽  
Epithelial Homeostasis ◽  
Cell Death Receptor

(1) We wanted to assess the prognostic impact of inflammasomes involved in gut epithelial homeostasis and the development of human colorectal cancer (CRC). (2) We investigated the expression of inflammasome components in colonic epithelial cells at the protein level in patient tissues, through an immunofluorescence assay. (3) In a cohort of 104 patients, we found that all inflammasome components were downregulated in CRC. Loss of epithelial (but not stromal) expression of NLRP6, caspase-1 and IL-18 was associated with an increased mortality of 72%, 58% and 68% respectively and to disease progression into metastasis. The loss of epithelial and stromal IL-18 but not NLRP6, was associated to lower tumor immune infiltrates in the lymphoid compartment and higher Programmed cell Death receptor 1 (PD-1) expression. Finally, we found that combined downregulation of IL-18 and NLRP6 was associated with a worse outcome. Indeed, 5-year survival rates were 26% for the NLRP6low/IL-18low tumors, compared to 64.4% for the entire cohort. This downregulation was associated with a more advanced disease (p < 0.0001) and a trend to lower lymphoid cell infiltration. (4) We identified critical inflammasome markers that may help in better stratifying patients for prognosis in CRC and could help clinicians to determine which patients may benefit from immunotherapies.

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