Matches in SemOpenAlex for { <https://semopenalex.org/work/W1851692042> ?p ?o ?g. }
- W1851692042 endingPage "4298" @default.
- W1851692042 startingPage "4287" @default.
- W1851692042 abstract "In this study, we have addressed the role of H(2)S in modulating neutrophil migration in either innate (LPS-challenged naive mice) or adaptive (methylated BSA (mBSA)-challenged immunized mice) immune responses. Treatment of mice with H(2)S synthesis inhibitors, dl-propargylglycine (PAG) or beta-cyanoalanine, reduced neutrophil migration induced by LPS or methylated BSA (mBSA) into the peritoneal cavity and by mBSA into the femur/tibial joint of immunized mice. This effect was associated with decreased leukocyte rolling, adhesion, and P-selectin and ICAM-1 expression on endothelium. Predictably, treatment of animals with the H(2)S donors, NaHS or Lawesson's reagent, enhanced these parameters. Moreover, the NaHS enhancement of neutrophil migration was not observed in ICAM-1-deficient mice. Neither PAG nor NaHS treatment changed LPS-induced CD18 expression on neutrophils, nor did the LPS- and mBSA-induced release of neutrophil chemoattractant mediators TNF-alpha, keratinocyte-derived chemokine, and LTB(4). Furthermore, in vitro MIP-2-induced neutrophil chemotaxis was inhibited by PAG and enhanced by NaHS treatments. Accordingly, MIP-2-induced CXCR2 internalization was enhanced by PAG and inhibited by NaHS treatments. Moreover, NaHS prevented MIP-2-induced CXCR2 desensitization. The PAG and NaHS effects correlated, respectively, with the enhancement and inhibition of MIP-2-induced G protein-coupled receptor kinase 2 expression. The effects of NaHS on neutrophil migration both in vivo and in vitro, together with CXCR2 internalization and G protein-coupled receptor kinase 2 expression were prevented by the ATP-sensitive potassium (K(ATP)(+)) channel blocker, glybenclamide. Conversely, diazoxide, a K(ATP)(+) channel opener, increased neutrophil migration in vivo. Together, our data suggest that during the inflammatory response, H(2)S augments neutrophil adhesion and locomotion, by a mechanism dependent on K(ATP)(+) channels." @default.
- W1851692042 created "2016-06-24" @default.
- W1851692042 creator A5006216810 @default.
- W1851692042 creator A5006994441 @default.
- W1851692042 creator A5022267898 @default.
- W1851692042 creator A5026715333 @default.
- W1851692042 creator A5028614370 @default.
- W1851692042 creator A5029813098 @default.
- W1851692042 creator A5030831755 @default.
- W1851692042 creator A5034907357 @default.
- W1851692042 creator A5036305303 @default.
- W1851692042 creator A5050378541 @default.
- W1851692042 creator A5054996958 @default.
- W1851692042 creator A5063552393 @default.
- W1851692042 creator A5080243666 @default.
- W1851692042 date "2008-09-15" @default.
- W1851692042 modified "2023-09-29" @default.
- W1851692042 title "Hydrogen Sulfide Augments Neutrophil Migration through Enhancement of Adhesion Molecule Expression and Prevention of CXCR2 Internalization: Role of ATP-Sensitive Potassium Channels" @default.
- W1851692042 cites W1496638723 @default.
- W1851692042 cites W1502384183 @default.
- W1851692042 cites W1549347261 @default.
- W1851692042 cites W1574929990 @default.
- W1851692042 cites W1583780928 @default.
- W1851692042 cites W1612149354 @default.
- W1851692042 cites W1764016564 @default.
- W1851692042 cites W1856081267 @default.
- W1851692042 cites W1866353544 @default.
- W1851692042 cites W1888068317 @default.
- W1851692042 cites W1968930699 @default.
- W1851692042 cites W1969823173 @default.
- W1851692042 cites W1970415114 @default.
- W1851692042 cites W1970915918 @default.
- W1851692042 cites W1971900596 @default.
- W1851692042 cites W1975087239 @default.
- W1851692042 cites W1977373788 @default.
- W1851692042 cites W1980654031 @default.
- W1851692042 cites W1984267035 @default.
- W1851692042 cites W1988297612 @default.
- W1851692042 cites W1991038715 @default.
- W1851692042 cites W1999100547 @default.
- W1851692042 cites W1999549405 @default.
- W1851692042 cites W2005121187 @default.
- W1851692042 cites W2008664596 @default.
- W1851692042 cites W2009746953 @default.
- W1851692042 cites W2018561422 @default.
- W1851692042 cites W2026301161 @default.
- W1851692042 cites W2028516053 @default.
- W1851692042 cites W2029491963 @default.
- W1851692042 cites W2032226212 @default.
- W1851692042 cites W2032445461 @default.
- W1851692042 cites W2038402742 @default.
- W1851692042 cites W2039905417 @default.
- W1851692042 cites W2051132536 @default.
- W1851692042 cites W2054873911 @default.
- W1851692042 cites W2057860005 @default.
- W1851692042 cites W2064134578 @default.
- W1851692042 cites W2064187556 @default.
- W1851692042 cites W2071106984 @default.
- W1851692042 cites W2071453138 @default.
- W1851692042 cites W2074149437 @default.
- W1851692042 cites W2083897855 @default.
- W1851692042 cites W2098262530 @default.
- W1851692042 cites W2107497694 @default.
- W1851692042 cites W2117289100 @default.
- W1851692042 cites W2118811017 @default.
- W1851692042 cites W2122438668 @default.
- W1851692042 cites W2136682979 @default.
- W1851692042 cites W2139466474 @default.
- W1851692042 cites W2140953825 @default.
- W1851692042 cites W2141610173 @default.
- W1851692042 cites W2153855328 @default.
- W1851692042 cites W2155081197 @default.
- W1851692042 cites W2164989387 @default.
- W1851692042 cites W2172253460 @default.
- W1851692042 cites W2321766814 @default.
- W1851692042 cites W2338245682 @default.
- W1851692042 cites W4254974372 @default.
- W1851692042 doi "https://doi.org/10.4049/jimmunol.181.6.4287" @default.
- W1851692042 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/18768887" @default.
- W1851692042 hasPublicationYear "2008" @default.
- W1851692042 type Work @default.
- W1851692042 sameAs 1851692042 @default.
- W1851692042 citedByCount "81" @default.
- W1851692042 countsByYear W18516920422012 @default.
- W1851692042 countsByYear W18516920422013 @default.
- W1851692042 countsByYear W18516920422014 @default.
- W1851692042 countsByYear W18516920422015 @default.
- W1851692042 countsByYear W18516920422016 @default.
- W1851692042 countsByYear W18516920422017 @default.
- W1851692042 countsByYear W18516920422018 @default.
- W1851692042 countsByYear W18516920422019 @default.
- W1851692042 countsByYear W18516920422020 @default.
- W1851692042 countsByYear W18516920422021 @default.
- W1851692042 countsByYear W18516920422022 @default.
- W1851692042 countsByYear W18516920422023 @default.
- W1851692042 crossrefType "journal-article" @default.
- W1851692042 hasAuthorship W1851692042A5006216810 @default.
- W1851692042 hasAuthorship W1851692042A5006994441 @default.