FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2100067998> ?p ?o ?g. }

• W2100067998 endingPage "no" @default.
• W2100067998 startingPage "no" @default.
• W2100067998 abstract "Chronic alcohol use results in many pathological effects including alcoholic liver disease (ALD). ALD pathogenesis requires endotoxemia. Our previous studies showed that increased intestinal permeability is the major cause of endotoxemia, and that this gut leakiness is dependent on alcohol stimulation of inducible nitric oxide synthase (iNOS) in both alcoholic subjects and rodent models of alcoholic steatohepatitis. The mechanism of the alcohol-induced, iNOS-mediated disruption of the intestinal barrier function is not known. We have recently shown that alcohol stimulates activation of the transcription factor Snail and biomarkers of epithelial mesenchymal transition. As activated Snail disrupts tight junctional proteins, we hypothesized that activation of Snail by iNOS might be one of the key signaling pathways mediating alcohol-stimulated intestinal epithelial cell hyperpermeability.We measured intestinal permeability in alcohol-fed C57BL/6 control and iNOS knockout (KO) mice, and measured Snail protein expression in the intestines of these mice. We then examined intestinal epithelial permeability using the Caco-2 cell model of the intestinal barrier ± small interfering RNA (siRNA) inhibition of Snail. We assessed Snail activation by alcohol in Caco-2 cells ± inhibition of iNOS with L-NIL or siRNA. Finally, we assessed Snail activation by alcohol ± inhibition with siRNA for p21-activated kinase (PAK1).Our data show that chronic alcohol feeding promotes intestinal hyperpermeability in wild-type BL/6, but not in iNOS KO mice. Snail protein expression was increased in the intestines of alcohol-treated wild-type mice, but not in iNOS KO mice. siRNA inhibition of Snail significantly inhibited alcohol-induced hyperpermeability in Caco-2 cell monolayers. Alcohol stimulation of Snail(pS246) activation was blocked by inhibition of iNOS with L-NIL or with siRNA. siRNA inhibition of PAK1 significantly inhibited alcohol-mediated activation of Snail in Caco-2 cells.Our data confirmed our prior results and further demonstrated that alcohol-induced gut leakiness in rodents and intestinal epithelial cell monolayers is iNOS dependent. Our data also support a novel role for Snail activation in alcohol-induced, iNOS-mediated intestinal hyperpermeability and that PAK1 is responsible for activation of Snail at Ser246 with alcohol stimulation. Identification of these mechanisms for alcohol-induced intestinal hyperpermeability may provide new therapeutic targets for prevention and treatment of alcohol-induced leaky gut, endotoxemia, and endotoxin-associated complications of alcoholism such as ALD." @default.
• W2100067998 created "2016-06-24" @default.
• W2100067998 creator A5002619544 @default.
• W2100067998 creator A5035792845 @default.
• W2100067998 creator A5062131424 @default.
• W2100067998 creator A5078294303 @default.
• W2100067998 creator A5078526337 @default.
• W2100067998 date "2011-04-01" @default.
• W2100067998 modified "2023-10-03" @default.
• W2100067998 title "Role of Snail Activation in Alcohol-Induced iNOS-Mediated Disruption of Intestinal Epithelial Cell Permeability" @default.
• W2100067998 cites W1949487746 @default.
• W2100067998 cites W1964081206 @default.
• W2100067998 cites W1968044382 @default.
• W2100067998 cites W1986300628 @default.
• W2100067998 cites W1986759033 @default.
• W2100067998 cites W1987817703 @default.
• W2100067998 cites W1990153938 @default.
• W2100067998 cites W1990856526 @default.
• W2100067998 cites W1990938548 @default.
• W2100067998 cites W1997234851 @default.
• W2100067998 cites W1999834438 @default.
• W2100067998 cites W2006444511 @default.
• W2100067998 cites W2009410973 @default.
• W2100067998 cites W2010377711 @default.
• W2100067998 cites W2012154760 @default.
• W2100067998 cites W2025314114 @default.
• W2100067998 cites W2030699054 @default.
• W2100067998 cites W2048278498 @default.
• W2100067998 cites W2049713116 @default.
• W2100067998 cites W2052147433 @default.
• W2100067998 cites W2055592943 @default.
• W2100067998 cites W2059771211 @default.
• W2100067998 cites W2063147214 @default.
• W2100067998 cites W2072138444 @default.
• W2100067998 cites W2074673544 @default.
• W2100067998 cites W2076583198 @default.
• W2100067998 cites W2080888904 @default.
• W2100067998 cites W2083790763 @default.
• W2100067998 cites W2087367170 @default.
• W2100067998 cites W2089180209 @default.
• W2100067998 cites W2095147460 @default.
• W2100067998 cites W2100047947 @default.
• W2100067998 cites W2105622812 @default.
• W2100067998 cites W2119331847 @default.
• W2100067998 cites W2130200374 @default.
• W2100067998 cites W2140373856 @default.
• W2100067998 cites W2140449647 @default.
• W2100067998 cites W2140551998 @default.
• W2100067998 cites W2144175661 @default.
• W2100067998 cites W2145002455 @default.
• W2100067998 cites W2147046708 @default.
• W2100067998 cites W2154589460 @default.
• W2100067998 cites W2159526033 @default.
• W2100067998 cites W2164572272 @default.
• W2100067998 cites W2165901622 @default.
• W2100067998 cites W2171862332 @default.
• W2100067998 doi "https://doi.org/10.1111/j.1530-0277.2011.01510.x" @default.
• W2100067998 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/3698619" @default.
• W2100067998 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/21535025" @default.
• W2100067998 hasPublicationYear "2011" @default.
• W2100067998 type Work @default.
• W2100067998 sameAs 2100067998 @default.
• W2100067998 citedByCount "23" @default.
• W2100067998 countsByYear W21000679982012 @default.
• W2100067998 countsByYear W21000679982014 @default.
• W2100067998 countsByYear W21000679982015 @default.
• W2100067998 countsByYear W21000679982016 @default.
• W2100067998 countsByYear W21000679982017 @default.
• W2100067998 countsByYear W21000679982019 @default.
• W2100067998 countsByYear W21000679982021 @default.
• W2100067998 countsByYear W21000679982022 @default.
• W2100067998 countsByYear W21000679982023 @default.
• W2100067998 crossrefType "journal-article" @default.
• W2100067998 hasAuthorship W2100067998A5002619544 @default.
• W2100067998 hasAuthorship W2100067998A5035792845 @default.
• W2100067998 hasAuthorship W2100067998A5062131424 @default.
• W2100067998 hasAuthorship W2100067998A5078294303 @default.
• W2100067998 hasAuthorship W2100067998A5078526337 @default.
• W2100067998 hasBestOaLocation W21000679982 @default.
• W2100067998 hasConcept C104317684 @default.
• W2100067998 hasConcept C126322002 @default.
• W2100067998 hasConcept C127716648 @default.
• W2100067998 hasConcept C134018914 @default.
• W2100067998 hasConcept C164659718 @default.
• W2100067998 hasConcept C170493617 @default.
• W2100067998 hasConcept C182704531 @default.
• W2100067998 hasConcept C185592680 @default.
• W2100067998 hasConcept C18903297 @default.
• W2100067998 hasConcept C203014093 @default.
• W2100067998 hasConcept C22615655 @default.
• W2100067998 hasConcept C2777214474 @default.
• W2100067998 hasConcept C2777575235 @default.
• W2100067998 hasConcept C2777622882 @default.
• W2100067998 hasConcept C2779965526 @default.
• W2100067998 hasConcept C2781071285 @default.
• W2100067998 hasConcept C519581460 @default.
• W2100067998 hasConcept C55493867 @default.
• W2100067998 hasConcept C67705224 @default.

• next