Matches in SemOpenAlex for { <https://semopenalex.org/work/W2938287273> ?p ?o ?g. }
- W2938287273 endingPage "1099" @default.
- W2938287273 startingPage "1088" @default.
- W2938287273 abstract "Objective— Vascular calcification is associated with high risk of cardiovascular events and mortality. Osteochondrogenic differentiation of vascular smooth muscle cells (VSMCs) is the major cellular mechanism underlying vascular calcification. Because tissue hypoxia is a common denominator in vascular calcification, we investigated whether hypoxia per se triggers osteochondrogenic differentiation of VSMCs. Approach and Results— We studied osteochondrogenic differentiation of human aorta VSMCs cultured under normoxic (21% O 2 ) and hypoxic (5% O 2 ) conditions. Hypoxia increased protein expression of HIF (hypoxia-inducible factor)-1α and its target genes GLUT1 (glucose transporter 1) and VEGFA (vascular endothelial growth factor A) and induced mRNA and protein expressions of osteochondrogenic markers, that is, RUNX2 (runt-related transcription factor 2), SOX9 (Sry-related HMG box-9), OCN (osteocalcin) and ALP (alkaline phosphatase), and induced a time-dependent calcification of the extracellular matrix of VSMCs. HIF-1 inhibition by chetomin abrogated the effect of hypoxia on osteochondrogenic markers and abolished extracellular matrix calcification. Hypoxia triggered the production of reactive oxygen species, which was inhibited by chetomin. Scavenging reactive oxygen species by N -acetyl cysteine attenuated hypoxia-mediated upregulation of HIF-1α, RUNX2, and OCN protein expressions and inhibited extracellular matrix calcification, which effect was mimicked by a specific hydrogen peroxide scavenger sodium pyruvate and a mitochondrial reactive oxygen species inhibitor rotenone. Ex vivo culture of mice aorta under hypoxic conditions triggered calcification which was inhibited by chetomin and N -acetyl cysteine. In vivo hypoxia exposure (10% O 2 ) increased RUNX2 mRNA levels in mice lung and the aorta. Conclusions— Hypoxia contributes to vascular calcification through the induction of osteochondrogenic differentiation of VSMCs in an HIF-1–dependent and mitochondria-derived reactive oxygen species–dependent manner." @default.
- W2938287273 created "2019-04-25" @default.
- W2938287273 creator A5050407464 @default.
- W2938287273 creator A5068207317 @default.
- W2938287273 creator A5068492212 @default.
- W2938287273 creator A5075376414 @default.
- W2938287273 creator A5076397370 @default.
- W2938287273 creator A5081690721 @default.
- W2938287273 date "2019-06-01" @default.
- W2938287273 modified "2023-10-17" @default.
- W2938287273 title "Hypoxia Triggers Osteochondrogenic Differentiation of Vascular Smooth Muscle Cells in an HIF-1 (Hypoxia-Inducible Factor 1)–Dependent and Reactive Oxygen Species–Dependent Manner" @default.
- W2938287273 cites W1547863599 @default.
- W2938287273 cites W1713906157 @default.
- W2938287273 cites W1899746275 @default.
- W2938287273 cites W1912237646 @default.
- W2938287273 cites W1932584694 @default.
- W2938287273 cites W1970882491 @default.
- W2938287273 cites W1972458423 @default.
- W2938287273 cites W1973994630 @default.
- W2938287273 cites W1975476522 @default.
- W2938287273 cites W1987117656 @default.
- W2938287273 cites W1987948630 @default.
- W2938287273 cites W1993170727 @default.
- W2938287273 cites W1997578486 @default.
- W2938287273 cites W2002660236 @default.
- W2938287273 cites W2006035096 @default.
- W2938287273 cites W2018948980 @default.
- W2938287273 cites W2020990962 @default.
- W2938287273 cites W2023822901 @default.
- W2938287273 cites W2024007562 @default.
- W2938287273 cites W2027705428 @default.
- W2938287273 cites W2028748749 @default.
- W2938287273 cites W2039207179 @default.
- W2938287273 cites W2044322920 @default.
- W2938287273 cites W2045123453 @default.
- W2938287273 cites W2046396317 @default.
- W2938287273 cites W2057302849 @default.
- W2938287273 cites W2058299847 @default.
- W2938287273 cites W2060166745 @default.
- W2938287273 cites W2069036891 @default.
- W2938287273 cites W2091719873 @default.
- W2938287273 cites W2097684284 @default.
- W2938287273 cites W2102206507 @default.
- W2938287273 cites W2107309737 @default.
- W2938287273 cites W2107708548 @default.
- W2938287273 cites W2109223610 @default.
- W2938287273 cites W2116703462 @default.
- W2938287273 cites W2121744013 @default.
- W2938287273 cites W2121860616 @default.
- W2938287273 cites W2125582907 @default.
- W2938287273 cites W2129265683 @default.
- W2938287273 cites W2135419608 @default.
- W2938287273 cites W2136529991 @default.
- W2938287273 cites W2147834547 @default.
- W2938287273 cites W2148413329 @default.
- W2938287273 cites W2150762378 @default.
- W2938287273 cites W2153376781 @default.
- W2938287273 cites W2157167939 @default.
- W2938287273 cites W2161877652 @default.
- W2938287273 cites W2161987121 @default.
- W2938287273 cites W2163408805 @default.
- W2938287273 cites W2166199725 @default.
- W2938287273 cites W2169952241 @default.
- W2938287273 cites W2172167693 @default.
- W2938287273 cites W2260144678 @default.
- W2938287273 cites W2413382674 @default.
- W2938287273 cites W2423642266 @default.
- W2938287273 cites W2481974289 @default.
- W2938287273 cites W2517631128 @default.
- W2938287273 cites W2553684564 @default.
- W2938287273 cites W2591395115 @default.
- W2938287273 cites W2611049315 @default.
- W2938287273 cites W2611954277 @default.
- W2938287273 cites W2621074013 @default.
- W2938287273 cites W4254763216 @default.
- W2938287273 doi "https://doi.org/10.1161/atvbaha.119.312509" @default.
- W2938287273 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/31070451" @default.
- W2938287273 hasPublicationYear "2019" @default.
- W2938287273 type Work @default.
- W2938287273 sameAs 2938287273 @default.
- W2938287273 citedByCount "55" @default.
- W2938287273 countsByYear W29382872732019 @default.
- W2938287273 countsByYear W29382872732020 @default.
- W2938287273 countsByYear W29382872732021 @default.
- W2938287273 countsByYear W29382872732022 @default.
- W2938287273 countsByYear W29382872732023 @default.
- W2938287273 crossrefType "journal-article" @default.
- W2938287273 hasAuthorship W2938287273A5050407464 @default.
- W2938287273 hasAuthorship W2938287273A5068207317 @default.
- W2938287273 hasAuthorship W2938287273A5068492212 @default.
- W2938287273 hasAuthorship W2938287273A5075376414 @default.
- W2938287273 hasAuthorship W2938287273A5076397370 @default.
- W2938287273 hasAuthorship W2938287273A5081690721 @default.
- W2938287273 hasBestOaLocation W29382872731 @default.
- W2938287273 hasConcept C104317684 @default.
- W2938287273 hasConcept C126322002 @default.
- W2938287273 hasConcept C134018914 @default.
- W2938287273 hasConcept C160450060 @default.