Complement C5a, TGF-β1, and MCP-1, in Sequence, Induce Migration of Monocytes Into Ischemic Canine Myocardium Within the First One to Five Hours After Reperfusion

Birdsall, Holly H.; Green, David M.; Trial, JoAnn; Youker, Keith A.; Burns, Alan R.; Mackay, Charles R.; LaRosa, Gregory J.; Hawkins, Hal K.; Smith, C. W.; Michael, Lloyd H.; Entman, Mark L.; Rossen, Roger D.

doi:10.1161/01.cir.95.3.684

Cited by 200 publications

(166 citation statements)

References 37 publications

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“…Recent investigations using experimental models of myocardial infarction demonstrated strong induction of several members of the chemokine family in the ischemic heart supporting their role in leukocyte recruitment [32], infarct angiogenesis and fibrous tissue deposition [96].…”

Section: The Chemokine Family In Myocardial Infarctionmentioning

confidence: 98%

“…Complement activation may play an important role in mediating neutrophil and monocyte recruitment in the injured myocardium [31]. The contribution of complement activation in mononuclear cell recruitment appears to be particularly important during the first hour of reperfusion [32].…”

Section: The Complement Cascadementioning

confidence: 99%

“…TGF-β expression is predominantly localized in the infarct border zone, associated with expression of Smad2, 3 and 4 [310] and phosphorylation of Smad1 and Smad2 [311]. Although evidence suggests that bioactive TGF-β is released in the cardiac extracellular fluids 3-5h following reperfused infarction [32], the mechanisms responsible for TGF-β activation in the infarcted heart are poorly understood. Our recent experiments suggested that TSP-1 induction in the infarct border zone may play an important role in activation of TGF-β signaling pathways in mouse and canine infarcts [312].…”

Section: Tgf-β Induction and Activation In Cardiac Injurymentioning

confidence: 99%

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The immune system and cardiac repair

Frangogiannis

2008

Pharmacological Research

568

499

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Myocardial infarction is the most common cause of cardiac injury and results in acute loss of a large number of myocardial cells. Because the heart has negligible regenerative capacity, cardiomyocyte death triggers a reparative response that ultimately results in formation of a scar and is associated with dilative remodeling of the ventricle. Cardiac injury activates innate immune mechanisms initiating an inflammatory reaction. Toll Like Receptor-mediated pathways, the complement cascade and reactive oxygen generation induce Nuclear Factor (NF)-κB activation and upregulate chemokine and cytokine synthesis in the infarcted heart. Chemokines stimulate the chemotactic recruitment of inflammatory leukocytes into the infarct, while cytokines promote adhesive interactions between leukocytes and endothelial cells, resulting in transmigration of inflammatory cells into the site of injury. Monocyte subsets play distinct roles in phagocytosis of dead cardiomyocytes and in granulation tissue formation through the release of growth factors. Clearance of dead cells and matrix debris may be essential for resolution of inflammation and transition into the reparative phase. Transforming Growth Factor (TGF)-β plays a crucial role in cardiac repair by suppressing inflammation while promoting myofibroblast phenotypic modulation and extracellular matrix deposition. Myofibroblast proliferation and angiogenesis result in formation of highly vascularized granulation tissue. As the healing infarct matures, fibroblasts become apoptotic and a collagen-based matrix is formed, while many infarct neovessels acquire a muscular coat and uncoated vessels regress. Timely resolution of the inflammatory infiltrate and spatial containment of the inflammatory and reparative response into the infarcted area are essential for optimal infarct healing. Targeting inflammatory pathways following infarction may reduce cardiomyocyte injury and attenuate adverse remodeling. In addition, understanding the role of the immune system in cardiac repair is necessary in order to design optimal strategies for cardiac regeneration.

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Section: The Chemokine Family In Myocardial Infarctionmentioning

confidence: 98%

Section: The Complement Cascadementioning

confidence: 99%

Section: Tgf-β Induction and Activation In Cardiac Injurymentioning

confidence: 99%

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The immune system and cardiac repair

Frangogiannis

2008

Pharmacological Research

568

499

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“…Reperfusion after ischemia can salvage the ischemic myocardium, however, simultaneously it causes additional cell death and attenuates the beneficial effects of reperfusion itself, called myocardial ischemia/reperfusion (I/R) injury [2]. Inflammation has been shown to play a critical role in the pathophysiology of myocardial I/R injury [3], and various immune cells, such as neutrophils, T lymphocytes, monocytes/macrophages, and mast cells, are involved in myocardial I/R injury [4][5][6][7]. Recent study by Yang et al demonstrated that CD4 + T lymphocytes played an important role in the development of I/R injury and interferon (IFN)-γ was involved in their action by using Rag1 knockout mice lacking mature lymphocytes [5].…”

Section: Introductionmentioning

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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“…2,3 Early reperfusion of the ischemic myocardium is a key clinical intervention after myocardial infarction and is attended by a robust inflammatory reaction involving both neutrophils and mononuclear cells. 5,6 It has been shown that late reperfusion, when myocardial salvage is no longer possible, improves myocardial repair and obviates infarct expansion. …”

mentioning

confidence: 99%

Reactive Oxygen Intermediates Induce Monocyte Chemotactic Protein-1 in Vascular Endothelium after Brief Ischemia

Lakshminarayanan

Lewallen

Frangogiannis

et al. 2001

The American Journal of Pathology

Self Cite

102

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Monocyte chemotactic protein (MCP)-1 is a member of the CC chemokine family and serves as a chemotactic factor for the recruitment of monocytes and subpopulations of T cells during inflammation. 1 It is induced by the proinflammatory cytokines interleukin (IL)-1␤ and tumor necrosis factor (TNF)-␣, as well as phorbol esters, which regulate its induction at the transcriptional level through the cooperative interaction of the transcription factors AP-1 and nuclear factor (NF)-B. 2-4 Specifically, in endothelial cells, IL-1␤, TNF-␣, and phorbol esters mediate human MCP-1 gene expression through the cooperative interaction of the NF-B binding site at Ϫ90 bp (relative to the start site) and the AP-1 binding site at Ϫ68 bp. 2,3 Early reperfusion of the ischemic myocardium is a key clinical intervention after myocardial infarction and is attended by a robust inflammatory reaction involving both neutrophils and mononuclear cells. 5,6 It has been shown that late reperfusion, when myocardial salvage is no longer possible, improves myocardial repair and obviates infarct expansion.

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Complement C5a, TGF-β1, and MCP-1, in Sequence, Induce Migration of Monocytes Into Ischemic Canine Myocardium Within the First One to Five Hours After Reperfusion

Abstract: Beginning in the first 60 minutes after reperfusion, C5a, TGF-beta 1, and MCP-1, acting sequentially, promote infiltration of monocytes into formerly ischemic myocardium. These events may promote the healing of myocardial injury facilitated by reperfusion.

Cited by 200 publications

References 37 publications

The immune system and cardiac repair

The immune system and cardiac repair

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

Reactive Oxygen Intermediates Induce Monocyte Chemotactic Protein-1 in Vascular Endothelium after Brief Ischemia

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