FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2734961519> ?p ?o ?g. }

• W2734961519 endingPage "114" @default.
• W2734961519 startingPage "101" @default.
• W2734961519 abstract "Altered permeability of the endothelial barrier in a variety of tissues has implications both in disease pathogenesis and treatment. Glucocorticoids are potent mediators of endothelial permeability, and this forms the basis for their heavily prescribed use as medications to treat ocular disease. However, the effect of glucocorticoids on endothelial barriers elsewhere in the body is less well studied. Here, we investigated glucocorticoid-mediated changes in endothelial flux of Adiponectin (Ad), a hormone with a critical role in diabetes. First, we used monolayers of endothelial cells in vitro and found that the glucocorticoid dexamethasone increased transendothelial electrical resistance and reduced permeability of polyethylene glycol (PEG, molecular weight 4000 Da). Dexamethasone reduced flux of Ad from the apical to basolateral side, measured both by ELISA and Western blotting. We then examined a diabetic rat model induced by treatment with exogenous corticosterone, which was characterized by glucose intolerance and hyperinsulinemia. There was no change in circulating Ad but less Ad protein in skeletal muscle homogenates, despite slightly higher mRNA levels, in diabetic vs control muscles. Dexamethasone-induced changes in Ad flux across endothelial monolayers were associated with alterations in the abundance of select claudin tight junction (TJ) proteins. shRNA-mediated knockdown of one such gene, claudin-7 , in HUVEC resulted in decreased TEER and increased adiponectin flux, confirming the functional significance of Dex-induced changes in its expression. In conclusion, our study identifies glucocorticoid-mediated reductions in flux of Ad across endothelial monolayers in vivo and in vitro . This suggests that impaired Ad action in target tissues, as a consequence of reduced transendothelial flux, may contribute to the glucocorticoid-induced diabetic phenotype." @default.
• W2734961519 created "2017-07-21" @default.
• W2734961519 creator A5002488895 @default.
• W2734961519 creator A5015779781 @default.
• W2734961519 creator A5019761985 @default.
• W2734961519 creator A5037793750 @default.
• W2734961519 creator A5055548172 @default.
• W2734961519 creator A5057223298 @default.
• W2734961519 creator A5063943500 @default.
• W2734961519 creator A5070111620 @default.
• W2734961519 creator A5075661431 @default.
• W2734961519 date "2017-08-01" @default.
• W2734961519 modified "2023-09-27" @default.
• W2734961519 title "Transendothelial movement of adiponectin is restricted by glucocorticoids" @default.
• W2734961519 cites W1498982214 @default.
• W2734961519 cites W1600793587 @default.
• W2734961519 cites W1850146802 @default.
• W2734961519 cites W1965391222 @default.
• W2734961519 cites W1968326337 @default.
• W2734961519 cites W1976319056 @default.
• W2734961519 cites W1978030502 @default.
• W2734961519 cites W1978651800 @default.
• W2734961519 cites W1979139803 @default.
• W2734961519 cites W1989536894 @default.
• W2734961519 cites W1993256170 @default.
• W2734961519 cites W2000422049 @default.
• W2734961519 cites W2010987575 @default.
• W2734961519 cites W2012879495 @default.
• W2734961519 cites W2015443649 @default.
• W2734961519 cites W2016610409 @default.
• W2734961519 cites W2016741997 @default.
• W2734961519 cites W2017916832 @default.
• W2734961519 cites W2021048256 @default.
• W2734961519 cites W2038171282 @default.
• W2734961519 cites W2042183801 @default.
• W2734961519 cites W2046147374 @default.
• W2734961519 cites W2052555925 @default.
• W2734961519 cites W2054210009 @default.
• W2734961519 cites W2057399508 @default.
• W2734961519 cites W2063439586 @default.
• W2734961519 cites W2072137305 @default.
• W2734961519 cites W2073955221 @default.
• W2734961519 cites W2076310317 @default.
• W2734961519 cites W2078163265 @default.
• W2734961519 cites W2084190789 @default.
• W2734961519 cites W2085517319 @default.
• W2734961519 cites W2089572539 @default.
• W2734961519 cites W2095022880 @default.
• W2734961519 cites W2097992625 @default.
• W2734961519 cites W2104276961 @default.
• W2734961519 cites W2104358275 @default.
• W2734961519 cites W2105640184 @default.
• W2734961519 cites W2107098584 @default.
• W2734961519 cites W2107331939 @default.
• W2734961519 cites W2116211129 @default.
• W2734961519 cites W2118228561 @default.
• W2734961519 cites W2119810088 @default.
• W2734961519 cites W2128485668 @default.
• W2734961519 cites W2135040607 @default.
• W2734961519 cites W2136678246 @default.
• W2734961519 cites W2143438409 @default.
• W2734961519 cites W2148146809 @default.
• W2734961519 cites W2150021754 @default.
• W2734961519 cites W2150056483 @default.
• W2734961519 cites W2153366902 @default.
• W2734961519 cites W2155723834 @default.
• W2734961519 cites W2155851535 @default.
• W2734961519 cites W2168380873 @default.
• W2734961519 cites W2168761911 @default.
• W2734961519 cites W2188384337 @default.
• W2734961519 cites W2282812563 @default.
• W2734961519 cites W2282930302 @default.
• W2734961519 cites W2395739198 @default.
• W2734961519 cites W2410681887 @default.
• W2734961519 cites W4237909399 @default.
• W2734961519 doi "https://doi.org/10.1530/joe-16-0363" @default.
• W2734961519 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/6231241" @default.
• W2734961519 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/28705835" @default.
• W2734961519 hasPublicationYear "2017" @default.
• W2734961519 type Work @default.
• W2734961519 sameAs 2734961519 @default.
• W2734961519 citedByCount "6" @default.
• W2734961519 countsByYear W27349615192019 @default.
• W2734961519 countsByYear W27349615192021 @default.
• W2734961519 countsByYear W27349615192022 @default.
• W2734961519 crossrefType "journal-article" @default.
• W2734961519 hasAuthorship W2734961519A5002488895 @default.
• W2734961519 hasAuthorship W2734961519A5015779781 @default.
• W2734961519 hasAuthorship W2734961519A5019761985 @default.
• W2734961519 hasAuthorship W2734961519A5037793750 @default.
• W2734961519 hasAuthorship W2734961519A5055548172 @default.
• W2734961519 hasAuthorship W2734961519A5057223298 @default.
• W2734961519 hasAuthorship W2734961519A5063943500 @default.
• W2734961519 hasAuthorship W2734961519A5070111620 @default.
• W2734961519 hasAuthorship W2734961519A5075661431 @default.
• W2734961519 hasBestOaLocation W27349615191 @default.
• W2734961519 hasConcept C123012128 @default.
• W2734961519 hasConcept C126322002 @default.

• next