Induction of Monocyte Chemoattractant Protein-1 in the Small Veins of the Ischemic and Reperfused Canine Myocardium

Kumar, Ajith G.; Ballantyne, Christie M.; Michael, Lloyd H.; Kukielka, Gilbert L.; Youker, Keith A.; Lindsey, Merry L.; Hawkins, Hal K.; Birdsall, Holly H.; Mackay, Charles R.; LaRosa, Gregory J.; Rossen, Roger D.; Smith, C. W.; Entman, Mark L.

doi:10.1161/01.cir.95.3.693

Cited by 156 publications

(119 citation statements)

References 27 publications

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“…10 In our previous studies with reperfused myocardial infarcts we demonstrated an important role for TNF-␣ as an upstream cytokine that was released from a preformed store in mast cells during ischemia 11 and showed that TNF-␣ could also induce endothelial cell MCP-1 expression. 8 Our studies also showed that cardiac lymph collected after reperfusion induced MCP-1 mRNA. This led us to hypothesize that TNF-␣ was responsible, at least in part, for MCP-1 induction after reperfusion of the infarcted myocardium; however, the assignment of this role to TNF-␣ did not explain the highly specific cellular localization of MCP-1 induction to the venular endothelium during early reperfusion.…”

supporting

confidence: 64%

“…8 We have demonstrated that this molecule is a chemotactic signal for mononuclear cell migration in the reperfused myocardial infarction 8,9 and others have demonstrated its potential role in angiogenesis. 10 In our previous studies with reperfused myocardial infarcts we demonstrated an important role for TNF-␣ as an upstream cytokine that was released from a preformed store in mast cells during ischemia 11 and showed that TNF-␣ could also induce endothelial cell MCP-1 expression.…”

mentioning

confidence: 96%

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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

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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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supporting

confidence: 64%

mentioning

confidence: 96%

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

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102

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“…23 Both processes appear to contribute independently to postischemic reperfusion injury: acute leukocyte adhesion has been correlated to myocardial stunning, a rapid functional detriment. 24 Delayed leukocyte accumulation causing functional detriment of the myocardium was relevant in experimental protocols, where acute leukocyte adhesion was effectively blocked, whereas subacute endothelial activation was not antagonized.…”

Section: Discussionmentioning

confidence: 99%

Retroinfusion of NFκB decoy oligonucleotide extends cardioprotection achieved by CD18 inhibition in a preclinical study of myocardial ischemia and retroinfusion in pigs

Kupatt¹,

Wichels²,

Deiss³

et al. 2002

Gene Ther

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“…In addition to its critical role in mononuclear cell recruitment, MCP-1 exerts important actions on nonhematopoietic cells, inducing angiogenic and arteriogenic effects [122] and modulating fibroblast phenotype and activity by increasing collagen expression and by regulating MMP synthesis [123]. MCP-1 upregulation has been demonstrated in a canine [124], a rat [125,126] and a mouse model [127] of experimental myocardial infarction. Studies from our laboratory demonstrated that MCP-1 −/− mice had decreased and delayed macrophage infiltration in the healing infarct and exhibited delayed replacement of injured cardiomyocytes with granulation tissue.…”

Section: Chemokines In Myocardial Infarctionmentioning

confidence: 99%

The immune system and cardiac repair

Frangogiannis

2008

Pharmacological Research

563

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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Induction of Monocyte Chemoattractant Protein-1 in the Small Veins of the Ischemic and Reperfused Canine Myocardium

Abstract: MCP-1 mRNA is induced in the endothelium of a specific class of small veins immediately after reperfusion. MCP-1 induction is confined to the previously ischemic area that has been reperfused. We suggest a significant role for MCP-1 in monocyte trafficking in the reperfused myocardium.

Cited by 156 publications

References 27 publications

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

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

Retroinfusion of NFκB decoy oligonucleotide extends cardioprotection achieved by CD18 inhibition in a preclinical study of myocardial ischemia and retroinfusion in pigs

The immune system and cardiac repair

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