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dc.contributor.authorBidinger, Bonnie
dc.contributor.authorTorres, Roxabella
dc.contributor.authorRossetti, Ronald G.
dc.contributor.authorBrown, Lisa
dc.contributor.authorBeltre, Rosa
dc.contributor.authorBurstein, Sumner H.
dc.contributor.authorLian, Jane B.
dc.contributor.authorStein, Gary S.
dc.contributor.authorZurier, Robert B.
dc.date2022-08-11T08:10:57.000
dc.date.accessioned2022-08-23T17:26:25Z
dc.date.available2022-08-23T17:26:25Z
dc.date.issued2003-08-19
dc.date.submitted2011-01-11
dc.identifier.citationClin Immunol. 2003 Aug;108(2):95-102.
dc.identifier.issn1521-6616 (Linking)
dc.identifier.pmid12921755
dc.identifier.urihttp://hdl.handle.net/20.500.14038/49633
dc.description.abstractOral administration of ajulemic acid (AjA), a synthetic nonpsychoactive cannabinoid acid, prevents joint cartilage and bone damage in an experimental model of arthritis in rats. Joint tissue injury in patients with rheumatoid arthritis (RA) is due in part to activation of T lymphocytes in the synovium, and T lymphocytes in synovium of RA patients are resistant to apoptosis. Thus, a potential mechanism whereby AjA prevents joint tissue injury in the animal model might be enhanced apoptosis of T lymphocytes. Apoptosis of human T cells in vitro was assessed by Annexin V expression, caspase-3 activity, DNA fragmentation, and microscopy. AjA induced apoptosis of T cells in a dose- and time-dependent manner. Apoptosis preceded loss of cell viability by trypan blue dye exclusion, confirming that cell loss was due to programmed cell death rather than necrosis. A nontoxic compound such as AjA may be a useful therapeutic agent for patients with diseases such as RA which are characterized by T-cell-driven chronic inflammation and tissue injury.
dc.language.isoen_US
dc.relation<a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&list_uids=12921755&dopt=Abstract">Link to Article in PubMed</a>
dc.relation.urlhttp://dx.doi.org/10.1016/S1521-6616(03)00064-0
dc.subjectAnnexin A5
dc.subjectAntirheumatic Agents
dc.subjectApoptosis
dc.subjectCaspase 3
dc.subjectCaspases
dc.subjectCell Division
dc.subjectCells, Cultured
dc.subjectDNA Fragmentation
dc.subjectDose-Response Relationship, Drug
dc.subjectFluorescein-5-isothiocyanate
dc.subjectHumans
dc.subjectMicroscopy, Fluorescence
dc.subjectMolecular Structure
dc.subjectT-Lymphocytes
dc.subjectTetrahydrocannabinol
dc.subjectCell Biology
dc.titleAjulemic acid, a nonpsychoactive cannabinoid acid, induces apoptosis in human T lymphocytes
dc.typeJournal Article
dc.source.journaltitleClinical immunology (Orlando, Fla.)
dc.source.volume108
dc.source.issue2
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/stein/60
dc.identifier.contextkey1724100
html.description.abstract<p>Oral administration of ajulemic acid (AjA), a synthetic nonpsychoactive cannabinoid acid, prevents joint cartilage and bone damage in an experimental model of arthritis in rats. Joint tissue injury in patients with rheumatoid arthritis (RA) is due in part to activation of T lymphocytes in the synovium, and T lymphocytes in synovium of RA patients are resistant to apoptosis. Thus, a potential mechanism whereby AjA prevents joint tissue injury in the animal model might be enhanced apoptosis of T lymphocytes. Apoptosis of human T cells in vitro was assessed by Annexin V expression, caspase-3 activity, DNA fragmentation, and microscopy. AjA induced apoptosis of T cells in a dose- and time-dependent manner. Apoptosis preceded loss of cell viability by trypan blue dye exclusion, confirming that cell loss was due to programmed cell death rather than necrosis. A nontoxic compound such as AjA may be a useful therapeutic agent for patients with diseases such as RA which are characterized by T-cell-driven chronic inflammation and tissue injury.</p>
dc.identifier.submissionpathstein/60
dc.contributor.departmentDepartment of Medicine
dc.contributor.departmentDepartment of Biochemistry and Molecular Pharmacology
dc.contributor.departmentDepartment of Cell Biology
dc.source.pages95-102


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