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- Ma, Li-Ping, et al.
(författare)
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Interleukin-6-deficient mice resist development of experimental autoimmune cardiomyopathy induced by immunization of β1-adrenergic receptor.
- 2012
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Ingår i: International journal of cardiology. - : Elsevier BV. - 1874-1754 .- 0167-5273. ; 155:1, s. 20-25
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND: IL-6 is known to be an important mediator in immune response and is now suggested to be involved in the pathogenesis of autoimmune diseases. However, little is known about the role of IL-6 in β(1)-adrenergic receptor induced autoimmune cardiomyopathy. MATERIALS AND METHODS: Twenty IL-6-deficient (IL-6(-/-)) mice and fifty-one wild type C57BL/6J (WT) mice were immunized with a synthetic peptide corresponding to the second extracellular loop of the β(1) (β(1)AR ECII) at 0, 1, 5, 9, 13weeks and observed until 25weeks. Another forty-one WT mice and twenty IL-6(-/-) mice were used as controls receiving vehicle in the same manner. RESULTS: As compared with IL-6(-/-) immunized and control mice, WT immunized mice showed increased end-systolic left ventricular dimension and end-diastolic left ventricular dimension as well as decreased fractional shortening and circumferential fiber shortening in the end of the experiment, which was accompanied by significantly increased antibody level. Moreover, mRNAs encoding for β(1)-adrenergic receptor kinase (GRK2), B-type natriuretic peptide (BNP) and β(1) adrenergic receptor (Adrb1) in heart tissues from WT immunized group were increased. There was a significant positive correlation among end-diastolic left ventricular dimension, autoantibody titer and mRNA expressions of BNP, Adrb1and GRK2. CONCLUSION: Our results demonstrated that immunization with β1AR ECII was unable to induce an early stage phenotype of cardiomyopathy in IL-6(-/-) mice, being different from wild type in which cardiomyopathy was observed, suggesting that IL-6 plays a key role in the regulation of β(1)AR induced autoimmune cardiomyopathy possibly through its enhanced antibody production.
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| 2. |
- Premaratne, Goditha U, et al.
(författare)
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Stromal Vascular Fraction Transplantation as an Alternative Therapy for Ischemic Heart Failure: Anti-inflammatory Role.
- 2011
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Ingår i: Journal of cardiothoracic surgery. - : Springer Science and Business Media LLC. - 1749-8090. ; 6
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Tidskriftsartikel (refereegranskat)abstract
- ABSTRACT: Background The aims of this study were: (1) to show the feasibility of using adipose-derived stromal vascular fraction (SVF) as an alternative to bone marrow mono nuclear cell (BM-MNC) for cell transplantation into chronic ischemic myocardium; and (2) to explore underlying mechanisms with focus on anti-inflammation role of engrafted SVF and BM-MNC post chronic myocardial infarction (MI) against left ventricular (LV) remodelling and cardiac dysfunction. Methods Four weeks after left ante rior descending coronary artery ligation, 32 Male Lewis rats with moderate MI were divided into 3 groups. SVF group (n = 12) had SVF cell transplantation (6 × 106 cells). BM-MNC group (n = 12) received BM-MNCs (6 × 106) and the control (n = 10) had culture medium. At 4 weeks, after the final echocardiography, histological sections were stained with Styrus red and immunohistochemical staining was performed for α-smooth muscle actin, von Willebrand factor, CD3, CD8 and CD20. Results At 4 weeks, in SVF and BM-MNC groups, LV diastolic dimension and LV systolic dimension were smaller and fractional shortening was increased in echocardiography, compared to control group. Histology revealed highest vascular density, CD3+ and CD20+ cells in SVF transplanted group. SVF transplantation decreased myocardial mRNA expression of inflammatory cytokines TNF-α, IL-6, MMP-1, TIMP-1 and inhibited collagen deposition. Conclusions Transplantation of adipose derived SVF cells might be a useful therapeutic option for angiogenesis in chronic ischemic heart disease. Anti-inflammation role for SVF and BM transplantation might partly benefit for the cardioprotective effect for chronic ischemic myocardium.
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