ArticleInflammatory bowel diseases2011
Protein kinase C iota in the intestinal epithelium protects against dextran sodium sulfate-induced colitis.
Article in Inflammatory bowel diseases, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 28 citations in OpenAlex.
- Role of MARK2 in the nervous system and cancer.Cancer gene therapy · 2024Review
- Protein kinase Cι mediates immunosuppression in lung adenocarcinoma.Science translational medicine · 2022Article
- Upregulation of OASIS/CREB3L1 in podocytes contributes to the disturbance of kidney homeostasis.Communications biology · 2022Article
- Article
- Fat of the Gut: Epithelial Phospholipids in Inflammatory Bowel Diseases.International journal of molecular sciences · 2021Review
- CD13 orients the apical-basal polarity axis necessary for lumen formation.Nature communications · 2021Article
- The cell polarity kinase Par1b/MARK2 activation selects specific NF-kB transcripts via phosphorylation of core mediator Med17/TRAP80.Molecular biology of the cell · 2021Article
- Mucosal Epithelial Jak Kinases in Health and Diseases.Mediators of inflammation · 2021Review
- Recurrent copy number gains drive PKCι expression and PKCι-dependent oncogenic signaling in human cancers.Advances in biological regulation · 2020Article
- Slit2/Robo1 Mitigates DSS-induced Ulcerative Colitis by Activating Autophagy in Intestinal Stem Cell.International journal of biological sciences · 2020Article
- The Dual Roles of the Atypical Protein Kinase Cs in Cancer.Cancer cell · 2019Review
- Eggshell membrane powder ameliorates intestinal inflammation by facilitating the restitution of epithelial injury and alleviating microbial dysbiosis.Scientific reports · 2017Article
- Soluble bioactive microbial mediators regulate proteasomal degradation and autophagy to protect against inflammation-induced stress.American journal of physiology. Gastrointestinal and liver physiology · 2016Article
- Control of Paneth Cell Fate, Intestinal Inflammation, and Tumorigenesis by PKCλ/ι.Cell reports · 2016Article
- Conditional knockout of polarity complex (atypical) PKCι reveals an anti-inflammatory function mediated by NF-κB.Molecular biology of the cell · 2016Article
- Changes in the phosphorylation of claudins during the course of experimental colitis.International journal of clinical and experimental pathology · 2015Article
- Regulation of polarized morphogenesis by protein kinase C iota in oncogenic epithelial spheroids.Carcinogenesis · 2014Article
- Protein kinase C zeta regulates human pancreatic cancer cell transformed growth and invasion through a STAT3-dependent mechanism.PloS one · 2013Article
- Article
- The role of innate immune-stimulated epithelial apoptosis during gastrointestinal inflammatory diseases.Cellular and molecular life sciences : CMLS · 2011Review
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
Abstract
backgroundThe integrity of the intestinal epithelium is critical for the absorption and retention of fluid and nutrients. The intestinal epithelium also provides a barrier between the intestinal bacteria and the body's immune surveillance. Therefore, intestinal epithelial barrier function is critically important, and disruption of the intestinal epithelium results in rapid repair of the damaged area.
methodsWe evaluated the requirement for protein kinase C iota (PKCι) in intestinal epithelial homeostasis and response to epithelial damage using a well-characterized mouse model of colitis. Mice were analyzed for the clinical, histological, and cellular effects of dextran sodium sulfate (DSS) treatment.
resultsKnockout of the mouse PKCι gene (Prkci) in the intestinal epithelium (Prkci KO mice) had no effect on normal colonic homeostasis; however, Prkci KO mice were significantly more sensitive to DSS-induced colitis and death. After withdrawal of DSS, Prkci KO mice exhibited a continued increase in apoptosis, inflammation, and damage to the intestinal microvasculature and a progressive loss of trefoil factor 3 (TFF3) expression, a regulatory peptide important for intestinal wound healing. Knockdown of PKCι expression in HT-29 cells reduced wound healing and TFF3 expression, while addition of exogenous TFF3 restored wound healing in PKCι-depleted cells.
conclusionsExpression of PKCι in the intestinal epithelium protects against DSS-induced colitis. Our data suggest that PKCι reduces DSS-induced damage by promoting intestinal epithelial wound healing through the control of TFF3 expression.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.