Abstract:
BACKGROUND:Peroxisome proliferator-activated receptor-gamma (PPAR-gamma) ligands have been shown to ameliorate a variety of inflammatory conditions. The present study tested the hypothesis that PPAR-gamma ligands reduce experimental autoimmune myocarditis (EAM) associated with inhibition of the expansion and activation of T cells, as well as suppression of the expression of proinflammatory cytokines. METHODS AND RESULTS:EAM was induced in Lewis rats by immunization with porcine cardiac myosin. PPAR-gamma ligands, 15-deoxy-Delta(12,14)-PGJ(2) (15d-PGJ(2)) 200 microg/kg/day i.p. and pioglitazone (PIO) 10 mg/kg/day orally, were administered for 3 weeks to rats with EAM. The results showed that enhanced PPAR-gamma expression was prominently stained in the nuclear and perinuclear regions of infiltrating inflammatory cells. Administration of PPAR-gamma ligands markedly reduced the severity of myocarditis, as shown by comparing the heart weight/body weight ratio, pericardial effusion scores, macroscopic scores and microscopic scores. PPAR-gamma ligands suppressed myocardial mRNA expression of inflammatory cytokines and the expression of interleukin (IL)-1beta protein in rats with EAM. In addition, 15d-PGJ(2) and PIO treatment suppressed the proliferative response and interferon-gamma production of T cell-enriched splenocytes from rats with EAM. Furthermore, the cytotoxic activity and myocardiogenic potential of these T cells were inhibited by 15d-PGJ(2) treatment. CONCLUSIONS:PPAR-gamma may play a role in the pathophysiology of EAM. PPAR-gamma ligands ameliorate the EAM associated with suppression of the expansion and activation of myocardiogenic T cells, as well as inhibition of the expression of proinflammatory cytokines. These results suggest that PPAR-gamma ligands such as 15d-PGJ(2) and PIO may have the potential to modulate human inflammatory heart diseases such as myocarditis.
journal_name
Cardiovasc Resjournal_title
Cardiovascular researchauthors
Yuan Z,Liu Y,Liu Y,Zhang J,Kishimoto C,Wang Y,Ma A,Liu Zdoi
10.1016/s0008-6363(03)00457-7subject
Has Abstractpub_date
2003-09-01 00:00:00pages
685-94issue
3eissn
0008-6363issn
1755-3245pii
S0008636303004577journal_volume
59pub_type
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journal_title:Cardiovascular research
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doi:10.1093/cvr/25.11.923
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journal_title:Cardiovascular research
pub_type: 杂志文章
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journal_title:Cardiovascular research
pub_type: 杂志文章
doi:10.1093/cvr/27.6.1033
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journal_title:Cardiovascular research
pub_type: 杂志文章
doi:10.1093/cvr/cvv204
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journal_title:Cardiovascular research
pub_type: 杂志文章
doi:10.1093/cvr/cvn308
更新日期:2009-02-01 00:00:00
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journal_title:Cardiovascular research
pub_type: 杂志文章
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更新日期:2011-12-01 00:00:00
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journal_title:Cardiovascular research
pub_type: 杂志文章,评审
doi:10.1016/j.cardiores.2004.02.010
更新日期:2004-05-01 00:00:00
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journal_title:Cardiovascular research
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doi:10.1093/cvr/27.5.817
更新日期:1993-05-01 00:00:00
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pub_type: 杂志文章
doi:10.1016/j.cardiores.2004.03.006
更新日期:2004-07-01 00:00:00
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journal_title:Cardiovascular research
pub_type: 杂志文章
doi:10.1016/s0008-6363(98)00345-9
更新日期:1999-07-01 00:00:00
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journal_title:Cardiovascular research
pub_type: 杂志文章,meta分析
doi:10.1093/cvr/cvy145
更新日期:2018-09-01 00:00:00
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journal_title:Cardiovascular research
pub_type: 杂志文章
doi:10.1016/s0008-6363(00)00187-5
更新日期:2000-12-01 00:00:00
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journal_title:Cardiovascular research
pub_type: 杂志文章,评审
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更新日期:2006-07-15 00:00:00
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doi:10.1016/j.cardiores.2004.10.019
更新日期:2005-02-15 00:00:00
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更新日期:1986-04-01 00:00:00
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pub_type: 杂志文章
doi:10.1093/cvr/13.6.338
更新日期:1979-06-01 00:00:00
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pub_type: 杂志文章
doi:10.1093/cvr/cvu033
更新日期:2014-04-01 00:00:00
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pub_type: 杂志文章
doi:10.1093/cvr/cvs281
更新日期:2012-12-01 00:00:00
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journal_title:Cardiovascular research
pub_type: 杂志文章
doi:10.1093/cvr/cvr158
更新日期:2011-10-01 00:00:00
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journal_title:Cardiovascular research
pub_type: 杂志文章
doi:10.1093/cvr/cvm049
更新日期:2008-01-01 00:00:00
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pub_type: 杂志文章,评审
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更新日期:2001-08-15 00:00:00
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pub_type: 杂志文章,评审
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更新日期:2009-02-15 00:00:00
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journal_title:Cardiovascular research
pub_type: 杂志文章
doi:10.1016/s0008-6363(01)00360-1
更新日期:2001-10-01 00:00:00