Matches in SemOpenAlex for { <https://semopenalex.org/work/W2024541610> ?p ?o ?g. }
- W2024541610 endingPage "2740" @default.
- W2024541610 startingPage "2731" @default.
- W2024541610 abstract "SIRT1 is known to inhibit apoptosis and to promote survival of various types of cells. However, the roles of SIRT1 in apoptosis of human chondrocytes have never been reported. We undertook this study to investigate the relationship of SIRT1 to apoptosis of human chondrocytes, which is a characteristic feature of osteoarthritis (OA).The expression of SIRT1 in human chondrocytes was examined by reverse transcription-polymerase chain reaction, immunoblotting, and immunohistology of human cartilage samples. The expression of SIRT1 under catabolic, mechanical, and nutritional stresses was investigated by immunoblotting. To examine the effect of SIRT1 on apoptosis, SIRT1 was inhibited by small interfering RNA (siRNA) and activated by resveratrol during nitric oxide (NO)-induced apoptosis. TUNEL staining and immunoblotting of cleaved poly(ADP-ribose) polymerase (PARP) were performed to detect apoptosis. To examine the mechanisms of apoptosis, we used immunoblotting to determine the levels of cleaved caspases and mitochondria-related apoptotic signaling proteins, Bax and Bcl-2, in the mitochondrial fraction.SIRT1 expression was confirmed in human chondrocytes and human cartilage samples. All catabolic, mechanical, and nutritional stresses inhibited SIRT1 expression. SIRT1 inhibition by siRNA for SIRT1 increased the percentage of TUNEL-positive cells and increased the amounts of cleaved PARP and cleaved caspases 3 and 9 induced by NO. In contrast, treatment with resveratrol decreased the percentage of TUNEL-positive cells and decreased the amounts of cleaved PARP and cleaved caspases 3 and 9 induced by NO. Furthermore, in the mitochondrial fraction, SIRT1 inhibition by siRNA for SIRT1 increased the amount of Bax but reduced the amount of Bcl-2, while resveratrol reduced the amount of Bax but increased the amount of Bcl-2.These results indicate that SIRT1 regulates apoptosis in human chondrocytes through the modulation of mitochondria-related apoptotic signals. Further research on SIRT1 might contribute to resolving the pathogenesis of OA." @default.
- W2024541610 created "2016-06-24" @default.
- W2024541610 creator A5001698830 @default.
- W2024541610 creator A5019321843 @default.
- W2024541610 creator A5022399570 @default.
- W2024541610 creator A5030625832 @default.
- W2024541610 creator A5046798526 @default.
- W2024541610 creator A5061929844 @default.
- W2024541610 creator A5064215891 @default.
- W2024541610 creator A5071471987 @default.
- W2024541610 creator A5076164909 @default.
- W2024541610 creator A5080712404 @default.
- W2024541610 creator A5083948998 @default.
- W2024541610 creator A5088758930 @default.
- W2024541610 date "2009-09-01" @default.
- W2024541610 modified "2023-10-02" @default.
- W2024541610 title "SIRT1 regulation of apoptosis of human chondrocytes" @default.
- W2024541610 cites W1963846930 @default.
- W2024541610 cites W1964059126 @default.
- W2024541610 cites W1967495700 @default.
- W2024541610 cites W1971877137 @default.
- W2024541610 cites W1973723400 @default.
- W2024541610 cites W1982879887 @default.
- W2024541610 cites W1986100120 @default.
- W2024541610 cites W1987738803 @default.
- W2024541610 cites W1998533677 @default.
- W2024541610 cites W2003611137 @default.
- W2024541610 cites W2004503111 @default.
- W2024541610 cites W2007451556 @default.
- W2024541610 cites W2010531594 @default.
- W2024541610 cites W2012753961 @default.
- W2024541610 cites W2014983456 @default.
- W2024541610 cites W2017356757 @default.
- W2024541610 cites W2017994898 @default.
- W2024541610 cites W2021958704 @default.
- W2024541610 cites W2024996523 @default.
- W2024541610 cites W2025746864 @default.
- W2024541610 cites W2031592383 @default.
- W2024541610 cites W2041999616 @default.
- W2024541610 cites W2042793067 @default.
- W2024541610 cites W2050177842 @default.
- W2024541610 cites W2053176849 @default.
- W2024541610 cites W2067694345 @default.
- W2024541610 cites W2073988218 @default.
- W2024541610 cites W2074740541 @default.
- W2024541610 cites W2078118441 @default.
- W2024541610 cites W2088381487 @default.
- W2024541610 cites W2095168835 @default.
- W2024541610 cites W2095712464 @default.
- W2024541610 cites W2097948853 @default.
- W2024541610 cites W2102635586 @default.
- W2024541610 cites W2106715610 @default.
- W2024541610 cites W2118204731 @default.
- W2024541610 cites W2119683782 @default.
- W2024541610 cites W2124595934 @default.
- W2024541610 cites W2135387645 @default.
- W2024541610 cites W2140925956 @default.
- W2024541610 cites W2145955296 @default.
- W2024541610 cites W2150494811 @default.
- W2024541610 cites W2157719302 @default.
- W2024541610 cites W2167990179 @default.
- W2024541610 cites W2168565631 @default.
- W2024541610 cites W2171391341 @default.
- W2024541610 cites W22650887 @default.
- W2024541610 doi "https://doi.org/10.1002/art.24864" @default.
- W2024541610 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/19714620" @default.
- W2024541610 hasPublicationYear "2009" @default.
- W2024541610 type Work @default.
- W2024541610 sameAs 2024541610 @default.
- W2024541610 citedByCount "184" @default.
- W2024541610 countsByYear W20245416102012 @default.
- W2024541610 countsByYear W20245416102013 @default.
- W2024541610 countsByYear W20245416102014 @default.
- W2024541610 countsByYear W20245416102015 @default.
- W2024541610 countsByYear W20245416102016 @default.
- W2024541610 countsByYear W20245416102017 @default.
- W2024541610 countsByYear W20245416102018 @default.
- W2024541610 countsByYear W20245416102019 @default.
- W2024541610 countsByYear W20245416102020 @default.
- W2024541610 countsByYear W20245416102021 @default.
- W2024541610 countsByYear W20245416102022 @default.
- W2024541610 countsByYear W20245416102023 @default.
- W2024541610 crossrefType "journal-article" @default.
- W2024541610 hasAuthorship W2024541610A5001698830 @default.
- W2024541610 hasAuthorship W2024541610A5019321843 @default.
- W2024541610 hasAuthorship W2024541610A5022399570 @default.
- W2024541610 hasAuthorship W2024541610A5030625832 @default.
- W2024541610 hasAuthorship W2024541610A5046798526 @default.
- W2024541610 hasAuthorship W2024541610A5061929844 @default.
- W2024541610 hasAuthorship W2024541610A5064215891 @default.
- W2024541610 hasAuthorship W2024541610A5071471987 @default.
- W2024541610 hasAuthorship W2024541610A5076164909 @default.
- W2024541610 hasAuthorship W2024541610A5080712404 @default.
- W2024541610 hasAuthorship W2024541610A5083948998 @default.
- W2024541610 hasAuthorship W2024541610A5088758930 @default.
- W2024541610 hasConcept C105702510 @default.
- W2024541610 hasConcept C153911025 @default.
- W2024541610 hasConcept C182979987 @default.