ArticleInflammation2013
Activation of RhoA in alcohol-induced intestinal barrier dysfunction.
Article in Inflammation, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
5 citing papers in PubMed, 9 citations in OpenAlex.
- Role of ROCK/NF‑κB/AQP8 signaling in ethanol‑induced intestinal epithelial barrier dysfunction.Molecular medicine reports · 2020Article
- RhoA/Rho-kinases in asthma: from pathogenesis to therapeutic targets.Clinical & translational immunology · 2020Review
- Dysregulation of junctional adhesion molecule-A contributes to ethanol-induced barrier disruption in intestinal epithelial cell monolayers.Physiological reports · 2017Article
- Obesogenic diet-induced gut barrier dysfunction and pathobiont expansion aggravate experimental colitis.PloS one · 2017Article
- Chronic Ethanol Exposure: Pathogenesis of Pulmonary Disease and Dysfunction.Biomolecules · 2015Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Ras homolog gene family, member A (RhoA) is a small GTPase protein known to regulate multiple cellular processes. In the present study, we used both an alcohol-fed mouse model and an alcohol-treated Caco-2 intestinal epithelial cell monolayer in vitro model to investigate whether RhoA is involved in alcohol-induced intestinal barrier dysfunction as well as the underlying mechanisms. We found that chronic alcohol exposure significantly increased both intestinal RhoA mRNA and protein levels in mice and alcohol treatment also increased RhoA activity in Caco-2 cells. The alcohol-induced elevation in RhoA activity was accompanied by an increase in inducible nitric oxide synthase (iNOS) expression and prevented by N⁶-(1-iminoethyl)-L-lysine dihydrochloride (L-NIL) or small interfering RNA (siRNA) specific for iNOS. Furthermore, alcohol treatment with Caco-2 cells resulted in a significant decrease in the epithelial transepithelial electrical resistance (TEER) value, which was attenuated by knockdown of RhoA. Taken together, our findings suggest that iNOS-mediated activation of RhoA appears to be one of the important mechanisms contributing to the deleterious effects of alcohol on intestinal barrier function.
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Registered trials
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.