FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2127984548> ?p ?o ?g. }

• W2127984548 endingPage "331" @default.
• W2127984548 startingPage "316" @default.
• W2127984548 abstract "Maintenance of the articular surface depends on the function of articular chondrocytes (ACs) which produce matrix and are constrained from undergoing the maturation program seen in growth plate chondrocytes. Only during pathologic conditions, such as in osteoarthritis, are maturational constraints lost causing recapitulation of the process that occurs during endochondral ossification. With the aim of establishing a model to identify regulatory mechanisms that suppress AC hypertrophy, we examined the capability of 5-azacytidine (Aza) to have an impact on the maturational program of these cells. Primary ACs do not spontaneously express markers of maturation and are refractory to treatment by factors that normally regulate chondrocyte maturation. However, following exposure to Aza, ACs (i) were induced to express type X collagen (colX), Indian hedgehog, and alkaline phosphatase and (ii) showed altered colX and AP expression in response to bone morphogenetic protein-2 (BMP-2), transforming growth factor-β (TGF-β), and parathyroid hormone-related protein (PTHrP). Since Aza unmasked responsiveness of ACs to BMP-2 and TGF-β, we examined the effect of Aza treatment on signaling via these pathways by assessing the expression of the TGF-β Smads (2 and 3), the BMP-2 Smads (1 and 5), and the Smad2 and 3-degrading ubiquitin E3 ligase Smurf2. Aza-treated ACs displayed less Smad2 and 3 and increased Smad1, 5, and Smurf2 protein and showed a loss of TGF-β signaling on the P3TP-luciferase reporter. Suggesting that Aza-induction of Smurf2 may be responsible for the loss of Smad2 and 3 protein via this pathway, immunoprecipitation and metabolic labeling experiments confirmed that Aza accelerated the ubiquitination and degradation of these targets. Overall, Aza-treated ACs represent a novel model for the study of mechanisms that regulate maturational potential of articular cartilage, with the data suggesting that maturation of these cells may be due to up-regulation of Smad1 and 5 coupled with a Smurf2-dependent degradation of Smad2 and 3 and loss of TGF-β signaling. © 2004 Wiley-Liss, Inc." @default.
• W2127984548 created "2016-06-24" @default.
• W2127984548 creator A5009934771 @default.
• W2127984548 creator A5024783120 @default.
• W2127984548 creator A5027291827 @default.
• W2127984548 creator A5027366738 @default.
• W2127984548 creator A5034940707 @default.
• W2127984548 creator A5040333932 @default.
• W2127984548 creator A5041375808 @default.
• W2127984548 creator A5058011844 @default.
• W2127984548 creator A5074891524 @default.
• W2127984548 date "2004-01-01" @default.
• W2127984548 modified "2023-10-14" @default.
• W2127984548 title "5-azacytidine alters TGF-? and BMP signaling and induces maturation in articular chondrocytes" @default.
• W2127984548 cites W1519258930 @default.
• W2127984548 cites W1528346173 @default.
• W2127984548 cites W1551310212 @default.
• W2127984548 cites W1637312052 @default.
• W2127984548 cites W1663371441 @default.
• W2127984548 cites W1948328269 @default.
• W2127984548 cites W1965344790 @default.
• W2127984548 cites W1971157583 @default.
• W2127984548 cites W1979208896 @default.
• W2127984548 cites W1986193321 @default.
• W2127984548 cites W1991424506 @default.
• W2127984548 cites W1992468405 @default.
• W2127984548 cites W1995499476 @default.
• W2127984548 cites W2003573512 @default.
• W2127984548 cites W2009396278 @default.
• W2127984548 cites W2009629707 @default.
• W2127984548 cites W2009915497 @default.
• W2127984548 cites W2016327551 @default.
• W2127984548 cites W2019303375 @default.
• W2127984548 cites W2021263701 @default.
• W2127984548 cites W2027782583 @default.
• W2127984548 cites W2029930661 @default.
• W2127984548 cites W2031726037 @default.
• W2127984548 cites W2033422116 @default.
• W2127984548 cites W2039386859 @default.
• W2127984548 cites W2043614517 @default.
• W2127984548 cites W2048885649 @default.
• W2127984548 cites W2050292154 @default.
• W2127984548 cites W2061798549 @default.
• W2127984548 cites W2063107258 @default.
• W2127984548 cites W2063141151 @default.
• W2127984548 cites W2063578899 @default.
• W2127984548 cites W2065977820 @default.
• W2127984548 cites W2067231965 @default.
• W2127984548 cites W2068868224 @default.
• W2127984548 cites W2072321739 @default.
• W2127984548 cites W2074346944 @default.
• W2127984548 cites W2085530184 @default.
• W2127984548 cites W2086013207 @default.
• W2127984548 cites W2090905598 @default.
• W2127984548 cites W2099669252 @default.
• W2127984548 cites W2101408271 @default.
• W2127984548 cites W2104283759 @default.
• W2127984548 cites W2109914347 @default.
• W2127984548 cites W2111602420 @default.
• W2127984548 cites W2116482468 @default.
• W2127984548 cites W2120960485 @default.
• W2127984548 cites W2123819897 @default.
• W2127984548 cites W2124377144 @default.
• W2127984548 cites W2144459502 @default.
• W2127984548 cites W2149718794 @default.
• W2127984548 cites W2151840099 @default.
• W2127984548 cites W2160013986 @default.
• W2127984548 cites W2162291763 @default.
• W2127984548 cites W2171894574 @default.
• W2127984548 cites W2480913198 @default.
• W2127984548 cites W4214729091 @default.
• W2127984548 cites W4234990183 @default.
• W2127984548 cites W4296588288 @default.
• W2127984548 cites W4378894981 @default.
• W2127984548 doi "https://doi.org/10.1002/jcb.20050" @default.
• W2127984548 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/15108358" @default.
• W2127984548 hasPublicationYear "2004" @default.
• W2127984548 type Work @default.
• W2127984548 sameAs 2127984548 @default.
• W2127984548 citedByCount "45" @default.
• W2127984548 countsByYear W21279845482012 @default.
• W2127984548 countsByYear W21279845482013 @default.
• W2127984548 countsByYear W21279845482014 @default.
• W2127984548 countsByYear W21279845482015 @default.
• W2127984548 countsByYear W21279845482017 @default.
• W2127984548 countsByYear W21279845482018 @default.
• W2127984548 countsByYear W21279845482019 @default.
• W2127984548 countsByYear W21279845482020 @default.
• W2127984548 countsByYear W21279845482022 @default.
• W2127984548 countsByYear W21279845482023 @default.
• W2127984548 crossrefType "journal-article" @default.
• W2127984548 hasAuthorship W2127984548A5009934771 @default.
• W2127984548 hasAuthorship W2127984548A5024783120 @default.
• W2127984548 hasAuthorship W2127984548A5027291827 @default.
• W2127984548 hasAuthorship W2127984548A5027366738 @default.
• W2127984548 hasAuthorship W2127984548A5034940707 @default.
• W2127984548 hasAuthorship W2127984548A5040333932 @default.
• W2127984548 hasAuthorship W2127984548A5041375808 @default.

• next