ArticleThe American journal of pathology2011
Endogenous prion protein attenuates experimentally induced colitis.
Article in The American journal of pathology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 28 citations in OpenAlex.
- An LRP1-binding motif in cellular prion protein replicates cell-signaling activities of the full-length protein.JCI insight · 2023Article
- CDK inhibitor Palbociclib targets STING to alleviate autoinflammation.EMBO reports · 2022Article
- A Soluble PrPJournal of immunology (Baltimore, Md. : 1950) · 2022Article
- Microglia in Prion Diseases: Angels or Demons?International journal of molecular sciences · 2020Review
- Decreased ω-6:ω-3 PUFA ratio attenuates ethanol-induced alterations in intestinal homeostasis, microbiota, and liver injury.Journal of lipid research · 2019Article
- Stimulator of interferon genes (STING) activation exacerbates experimental colitis in mice.Scientific reports · 2019Article
- Oral Prion Neuroinvasion Occurs Independently of PrPJournal of virology · 2018Article
- Stress Resilience of Spermatozoa and Blood Mononuclear Cells without Prion Protein.Frontiers in molecular biosciences · 2018Article
- Prion protein is required for tumor necrosis factor α (TNFα)-triggered nuclear factor κB (NF-κB) signaling and cytokine production.The Journal of biological chemistry · 2017Article
- LPS-induced systemic inflammation reveals an immunomodulatory role for the prion protein at the blood-brain interface.Journal of neuroinflammation · 2017Article
- Goats without Prion Protein Display Enhanced Proinflammatory Pulmonary Signaling and Extracellular Matrix Remodeling upon Systemic Lipopolysaccharide Challenge.Frontiers in immunology · 2017Article
- The Cellular Prion Protein: A Player in Immunological Quiescence.Frontiers in immunology · 2015Review
- Cellular prion protein (PrP(C)) and its role in stress responses.International journal of clinical and experimental medicine · 2015Article
- Article
- Roles of the cellular prion protein in the regulation of cell-cell junctions and barrier function.Tissue barriers · 2013Review
- Article
- Continuous production of prions after infectious particles are eliminated: implications for Alzheimer's disease.PloS one · 2012Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Although the cellular prion protein (PrP(C)) is expressed in the enteric nervous system and lamina propria, its function(s) in the gut is unknown. Because PrP(C) may exert a cytoprotective effect in response to various physiologic stressors, we hypothesized that PrP(C) expression levels might modulate the severity of experimental colitis. We evaluated the course of dextran sodium sulfate (DSS)-induced colitis in hemizygous Tga20 transgenic mice (approximately sevenfold overexpression of PrP(C)), Prnp(-/-) mice, and wild-type mice. On day 7, colon length, disease severity, and histologic activity indices were determined. Unlike DSS-treated wild-type and Prnp(-/-) animals, PrP(C) overexpressing mice were resistant to colitis induction, exhibited much milder histopathologic features, and did not exhibit weight loss or colonic shortening. In keeping with these results, pro-survival molecule expression and/or phosphorylation levels were elevated in DSS-treated Tga20 mice, whereas pro-inflammatory cytokine production and pSTAT3 levels were reduced. In contrast, DSS-treated Prnp(-/-) mice exhibited increased BAD protein expression and a cytokine expression profile predicted to favor inflammation and differentiation. PrP(C) expression from both the endogenous Prnp locus or the Tga20 transgene was increased in the colons of DSS-treated mice. Considered together, these findings demonstrate that PrP(C) has a previously unrecognized cytoprotective and/or anti-inflammatory function within the murine colon.
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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.