Full metadata record
DC Field | Value | Language |
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dc.contributor.author | 윤영대 | - |
dc.date.accessioned | 2016-08-28T11:08:34Z | - |
dc.date.available | 2016-08-28T11:08:34Z | - |
dc.date.issued | 2004 | - |
dc.identifier.issn | 0022-1767 | - |
dc.identifier.other | OAK-1771 | - |
dc.identifier.uri | https://dspace.ewha.ac.kr/handle/2015.oak/219361 | - |
dc.description.abstract | Apoptosis is one way of controlling immune responses, and a variety of immunosuppressive drugs suppress harmful immune responses by inducing apoptosis of lymphocytes. In this study we observed that rosmarinic acid, a secondary metabolite of herbal plants, induced apoptosis in an p56lck (Lck)-dependent manner; Lck+ Jurkat T cells undergo apoptosis in response to rosmarinic acid (RosA) treatment, whereas Lck- Jurkat subclone J. CaM1.6 cells do not. J.CaM1.6 cells with various Lck mutants indicated that Lck SH2 domain, but not Lck kinase activity, was required for RosA-induced apoptosis. RosA induced apoptosis in the absence of a TCR stimulus, and this was not prevented by interruption of the Fas/Fas ligand interaction. Instead, RosA-mediated apoptosis involved a mitochondrial pathway as indicated by cytochrome c release and the complete blockage of apoptosis by an inhibitor of mitochondrial membrane depolarization. Both caspase-3 and -8 were indispensable in RosA-induced apoptosis and work downstream of mitochondria and caspase-9 in the order of caspase-9/caspase-3/caspase-8. In freshly isolated human PBMC, RosA specifically induced apoptosis of Lck+ subsets such as T and NK cells, but not Lck-deficient cells, including B cells and monocytes. Moreover, RosA's ability to kill T and NK cells was restricted to actively proliferating cells, but not to resting cells. In conclusion, Lck-dependent apoptotic activity may make RosA an attractive therapeutic tool for the treatment of diseases in which T cell apoptosis is beneficial. | - |
dc.language | English | - |
dc.title | Rosmarinic Acid Induces p56lck-Dependent Apoptosis in Jurkat and Peripheral T Cells via Mitochondrial Pathway Independent from Fas/Fas Ligand Interaction | - |
dc.type | Article | - |
dc.relation.issue | 1 | - |
dc.relation.volume | 172 | - |
dc.relation.index | SCIE | - |
dc.relation.index | SCOPUS | - |
dc.relation.startpage | 79 | - |
dc.relation.lastpage | 87 | - |
dc.relation.journaltitle | Journal of Immunology | - |
dc.identifier.wosid | WOS:000187427700014 | - |
dc.identifier.scopusid | 2-s2.0-0346734197 | - |
dc.author.google | Hur Y.-G. | - |
dc.author.google | Yun Y. | - |
dc.author.google | Won J. | - |
dc.contributor.scopusid | 윤영대(7201731033) | - |
dc.date.modifydate | 20200901081003 | - |