Cardioprotective effect of interleukin-10 in murine myocardial ischemia-reperfusion

Hayward, Reid; Nossuli, Tareck O.; Scalia, Rosario; Lefer, Allan M.

doi:10.1016/s0014-2999(97)01149-7

Cited by 54 publications

(41 citation statements)

References 35 publications

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“…Although, IL-10 has been shown to target neutrophils, specifically promoting neutrophil apoptosis, 13,34,35 we observed no difference in MPO activity, an indirect measurement of neutrophil number, and no difference in the number of immunohistochemically-detected neutrophils at day 1 or day 4 after MI between hearts injected with BM-MNCs or diluent. This result contrasts with previous studies where exogenously administered IL-10 led to a decrease in MPO activity after 20 minutes of ischemia followed by 24 hours reperfusion, 15 and where subjecting IL-10 -deficient mice to 30 minutes of ischemia followed by 6 hours of reperfusion led to an increase in MPO activity. 14 Alternatively, our data are consistent with a previous study showing no differences in neutrophil infiltration or resolution in IL-10 -deficient mice subjected to myocardial ischemia reperfusion.…”

Section: Discussioncontrasting

confidence: 99%

“…Indeed, IL-10 enhances resolution of pulmonary inflammation in vivo by promoting apoptosis of neutrophils, 13 and IL-10 -deficient mice revealed increased neutrophil infiltration, infarct size, and myocardial necrosis after acute MI. 14 Furthermore, IL-10 exogenously administered into rats 15 minutes before reperfusion significantly attenutated myocardial injury, 15 and elevated serum levels of IL-10 are associated with a more favorable prognosis in patients with acute coronary syndromes. 16 -18 Conversely, it has been shown that infarcted IL-10 -deficient mice showed no differences in neutrophil infiltration, infarct healing.…”

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confidence: 99%

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Interleukin-10 From Transplanted Bone Marrow Mononuclear Cells Contributes to Cardiac Protection After Myocardial Infarction

Burchfield

Iwasaki

Koyanagi

et al. 2008

Circulation Research

144

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Abstract-Bone marrow mononuclear cells (BM-MNCs) have successfully been used as a therapy for the improvement of left ventricular (LV) function after myocardial infarction (MI). It has been suggested that paracrine factors from BM-MNCs may be a key mechanism mediating cardiac protection. We previously performed microarray analysis and found that the pleiotropic cytokine interleukin (IL)-10 was highly upregulated in human progenitor cells in comparison with adult endothelial cells and CD14 ϩ cells. Moreover, BM-MNCs secrete significant amounts of IL-10, and IL-10 could be detected from progenitor cells transplanted in infarcted mouse hearts. Specifically, intramyocardial injection of wild-type BM-MNCs led to a significant decrease in LV end-diastolic pressure (LVEDP) and LV end-systolic volume (LVESV) compared to hearts injected with either diluent or IL-10 knock-out BM-MNCs. Furthermore, intramyocardial injection of wild-type BM-MNCs led to a significant increase in stroke volume (SV) and rate of the development of pressure over time (ϩdP/dt) compared to hearts injected with either diluent or IL-10 knock-out BM-MNCs. The IL-10 -dependent improvement provided by transplanted cells was not caused by reduced infarct size, neutrophil infiltration, or capillary density, but rather was associated with decreased T lymphocyte accumulation, reactive hypertrophy, and myocardial collagen deposition. These results suggest that BM-MNCs mediate cardiac protection after myocardial infarction and this is, at least in part, dependent on IL-10. Key Words: acute myocardial infarction Ⅲ remodeling Ⅲ growth factors/cytokines Ⅲ cell therapy B one marrow-derived progenitor cells have been used clinically to improve left ventricular (LV) function in patients after acute myocardial infarction (MI), 1-4 however the exact mechanisms for this improvement in cardiac function have not clearly been defined. Several mechanisms have been proposed to explain the beneficial effects of this cell-based therapy including cell transdifferentiation, cell fusion, and the release of paracrine growth factors and cytokines. In support of the latter mechanism, various cytokines and growth factors from transplanted progenitor cells have been shown to be important in progenitor cell-mediated cardiac protection such as basic fibroblast growth factor, vascular endothelial growth factor, stromal-derived factor, 5,6 angiopoietin-1, interleukin (IL)-1␤, tumor necrosis factor-␣, 7,8 hepatocyte growth factor, insulin-like growth factor-1, thymosin ␤4, 8 secreted frizzled related protein 2, 9 IL-6, placental growth factor, transforming growth factor, monocyte chemoattractant protein-1, platelet-derived growth factor, plasminogen activator, and metalloproteinase-9. 10 We previously performed microarray analysis on peripheral blood-derived cultured human precursor cells 11 and found one paracrine factor highly expressed, the pleiotropic cytokine, IL-10. IL-10 is expressed and secreted by a variety of cell types such as T cells, monocytes/macrophages, dendritic cells, ...

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Section: Discussioncontrasting

confidence: 99%

mentioning

confidence: 99%

Interleukin-10 From Transplanted Bone Marrow Mononuclear Cells Contributes to Cardiac Protection After Myocardial Infarction

Burchfield

Iwasaki

Koyanagi

et al. 2008

Circulation Research

144

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“…38,40 Transfected viral IL-10 decreases leukocyte vein extravasation through a decrease in endothelial expression of P-and E-selectin and ICAM-1. 40 IL-10 similarly blunts inflammation secondary to myocardial ischemia/reperfusion through an ICAM-1-dependent mechanism 44 and reduces liver injury and mortality in a mouse septic shock model through decreased neutrophil margination and ICAM-1 and VCAM-1 expression. 45 Endogenous IL-10 might also be produced during myocardial ischemia-reperfusion by lymphocytes infiltrating the reperfused myocardium and could limit myocardial macrophage activation.…”

Section: Il-10mentioning

confidence: 97%

Anti-Inflammatory Mechanisms in the Vascular Wall

Tedgui

Mallat

2001

Circulation Research

378

258

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Abstract-The role of vascular cells during inflammation is critical and is of particular importance in inflammatorydiseases, including atherosclerosis, ischemia/reperfusion, and septic shock. Research in vascular biology has progressed remarkably in the last decade, resulting in a better understanding of the vascular cell responses to inflammatory stimuli. Most of the vascular inflammatory responses are mediated through the IB/nuclear factor-B system. Much recent work shows that vascular inflammation can be limited by anti-inflammatory counteregulatory mechanisms that maintain the integrity and homeostasis of the vascular wall. The anti-inflammatory mechanisms in the vascular wall involve anti-inflammatory external signals and intracellular mediators. The anti-inflammatory external signals include the anti-inflammatory cytokines, transforming growth factor-␤, interleukin-10 and interleukin-1 receptor antagonist, HDL, as well as some angiogenic and growth factors. Physiological laminar shear stress is of particular importance in protecting endothelial cells against inflammatory activation. Its effects are partly mediated through NO production. Finally, endogenous cytoprotective genes or nuclear receptors, such as the peroxisome proliferator-activated receptors, can be expressed by vascular cells in response to proinflammatory stimuli to limit the inflammatory process and the injury. nflammation is a basic pathological mechanism that underlies a variety of diseases. The inflammatory reaction involves the complex interactions between inflammatory cells (neutrophils, lymphocytes, and monocytes/macrophages) and vascular cells (endothelial cells [ECs] and smooth muscle cells [SMCs]). The role of vascular cells during the inflammatory process is critical. Multiple cytokines and growth factors are present at sites of inflammation, and each of these can potentially influence the nature of the inflammatory response. ECs and SMCs must integrate the signals generated by these multiple factors to effectively regulate the immunoinflammatory response through the expression of adhesion molecules, cytokines, chemokines, matrix metalloproteinases, and growth factors. Research in vascular biology has progressed remarkably in the last decade, resulting in a better understanding of the vascular cell responses to inflammatory stimuli and resulting in the identification of major intracellular inflammatory signaling pathways, particularly the IB/nuclear factor-B (NF-B) system. Much recent work shows that vascular inflammation can be limited by anti-inflammatory counteregulatory mechanisms that maintain the integrity and homeostasis of the vascular wall. This might be of particular importance in inflammatory diseases, such as atherosclerosis, septic shock, or ischemia/reperfusion. The purpose of the present review is to describe recent advances in the understanding of the anti-inflammatory mechanisms in vascular cells, focusing on anti-inflammatory external signals and intracellular mediators Original

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“…Endogenous TNF-α and IL-1 play as a mediator of inflammatory reactions, whereas, IL-10 and TGF-β have cardioprotective effects on myocardial I/R injury. Previous studies demonstrated that the blocking of pro-inflammatory cytokines or the administration of cardioprotective cytokines reduced infarct size [32][33][34][35][36][37]. On the other hand, the increases in IL-4 and IFN-γ are characteristic of the activation of iNKT cells [9].…”

Section: Myocardial I/r Injury and Cytokinesmentioning

confidence: 99%

“…IL-10 has been reported to suppress the expression of CC chemokine gene including MCP-1 [40]. Exogenous IL-10 administration ameliorates myocardial I/R injury by inhibiting adherence of leukocytes to vascular endothelium [35], and by decreasing the production of pro-inflammatory cytokines through Signal Transducers and Activator of Transcription (STAT)-3 pathway [36]. It has also been shown that remote ischemic preconditioning has protective effects against myocardial I/R injury by the upregulation of IL-10 in the remote muscle and the release into circulation [41].…”

Section: Protective Effects Of Il-10 On Myocardial I/r Injurymentioning

confidence: 99%

Activation of invariant natural killer T cells by α-galactosylceramide ameliorates myocardial ischemia/reperfusion injury in mice

Homma¹,

Kinugawa²,

Takahashi³

et al. 2013

Journal of Molecular and Cellular Cardiology

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Cardioprotective effect of interleukin-10 in murine myocardial ischemia-reperfusion

Cited by 54 publications

References 35 publications

Interleukin-10 From Transplanted Bone Marrow Mononuclear Cells Contributes to Cardiac Protection After Myocardial Infarction

Interleukin-10 From Transplanted Bone Marrow Mononuclear Cells Contributes to Cardiac Protection After Myocardial Infarction

Anti-Inflammatory Mechanisms in the Vascular Wall

Activation of invariant natural killer T cells by α-galactosylceramide ameliorates myocardial ischemia/reperfusion injury in mice

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