Coronary endothelial P-selectin in pathogenesis of myocardial ischemia-reperfusion injury

Palazzo, Anthony J.; Jones, Steven P.; Anderson, Donald C.; Granger, D. Neil; Lefer, David J.

doi:10.1152/ajpheart.1998.275.5.h1865

Cited by 54 publications

(60 citation statements)

References 32 publications

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“…Experimental studies have suggested that monoclonal antibodies against L-selectin and P-selectin [183,184] reduced myocardial necrosis, preserving coronary endothelial function and attenuating neutrophil accumulation in the ischemic and reperfused feline myocardium. In addition, P-selectin deficient mice showed decreased infarct size after 30 min of coronary occlusion and 2 h of reperfusion [185]. In contrast, no difference in infarct size was noted after a 60 min ischemic period [185].…”

Section: The Neutrophilsmentioning

confidence: 99%

“…In addition, P-selectin deficient mice showed decreased infarct size after 30 min of coronary occlusion and 2 h of reperfusion [185]. In contrast, no difference in infarct size was noted after a 60 min ischemic period [185]. In addition, mice with a combined P-selectin and ICAM-1 deficiency demonstrated impaired neutrophil trafficking without a difference in infarct size due to myocardial ischemia and reperfusion [186].…”

Section: The Neutrophilsmentioning

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 Neutrophilsmentioning

confidence: 99%

Section: The Neutrophilsmentioning

confidence: 99%

The immune system and cardiac repair

Frangogiannis

2008

Pharmacological Research

568

499

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“…Recent studies have shown that myocardial ischemia/ reperfusion injury could be suppressed by preventing PMN accumulation by inhibition of P-selectin, L-selectin, ICAM-1, or CD18, which are leukocyte adhesion receptors or cell adhesion molecules. For example, the sizes of myocardial infarcts elicited by ischemia/reperfusion were diminished in P-selectin-deficient, ICAM-1-deficient, or CD18-deficient mice (46,47). In addition, ischemia/ reperfusion-induced PMN infiltration and myocardial infarct size were both diminished in dogs treated with a monoclonal anti-P-selectin Ab (48), and myocardial ischemia/reperfusion injuries were reduced by monoclonal Ab's directed against leukocyte adhesion receptor or cell adhesion molecules (49)(50)(51).…”

mentioning

confidence: 99%

Blockade of the natriuretic peptide receptor guanylyl cyclase-A inhibits NF-κB activation and alleviates myocardial ischemia/reperfusion injury

Izumi

Saito

Kishimoto³

et al. 2001

J. Clin. Invest.

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Acute myocardial infarction (AMI) remains the leading cause of death in developed countries. Although reperfusion of coronary arteries reduces mortality, it is associated with tissue injury. Endothelial P-selectin-mediated infiltration of neutrophils plays a key role in reperfusion injury. However, the mechanism of the P-selectin induction is not known. Here we show that infarct size after ischemia/reperfusion was significantly smaller in mice lacking guanylyl cyclase-A (GC-A), a natriuretic peptide receptor. The decrease was accompanied by decreases in neutrophil infiltration in coronary endothelial P-selectin expression. Pretreatment with HS-142-1, a GC-A antagonist, also decreased infarct size and P-selectin induction in wild-type mice. In cultured endothelial cells, activation of GC-A augmented H 2 O 2 -induced P-selectin expression. Furthermore, ischemia/reperfusion-induced activation of NF-κB, a transcription factor that is known to promote P-selectin expression, is suppressed in GC-A-deficient mice. These results suggest that inhibition of GC-A alleviates ischemia/reperfusion injury through suppression of NF-κB-mediated P-selectin induction. This novel, GC-A-mediated mechanism of ischemia/reperfusion injury may provide the basis for applying GC-A blockade in the clinical treatment of reperfusion injury. uretic peptide signaling on the size of myocardial infarcts evoked by protocols of ischemia and reperfusion. Methods Animals. GC-A-deficient (GC-A -/-) mice and their GC-A +/+littermates (wild-type controls) were generated as described previously (26). All mice used in this study were between 10 and 14 weeks old. C57BL/6 (10-14 weeks) mice were purchased from Shimizu Co. (Kyoto, Japan). All experimental procedures were performed according to Kyoto University standards for animal care.Surgical procedures. Mice were initially anesthetized with ether and placed on a warm pad maintained at 37°C. The trachea of each mouse was cannulated with a polyethylene tube connected to a respirator (Shinano Co., Tokyo, Japan) with a tidal volume set at 0.6 ml and a rate set at 110/min. The mice were then anesthetized with 0.5-1.5% isoflurane for the remainder of the surgical procedure. After a 10-minute equilibration period, a left thoracotomy was performed between the fourth and fifth ribs. The pericardial sac was then removed, and the left anterior descending artery (LAD) was visualized under a microscope and ligated with a 7-0 silk suture using a snare occluder. To avoid injuring the LAD, a small patch was attached to its surface. Ischemia and reperfusion were accomplished by first tightening the snare occluder and then loosening it. Significant electrocardiogram and color changes at the area at risk (AAR) were considered indicative of successful coronary occlusion and reperfusion. The silk suture was left in place, and chests of the mice were closed with 5-0 silk sutures. The animals were then weaned from the respirator, and the intratracheal tube was removed once they were breathing spontaneously and began to move.Myo...

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“…It has been indicated that endothelial injury/activation leads to the production of certain factors that release P-selectin of endothelial intracellular storage, which mediates cell adhesion [42,43]. Furthermore, the angiopoietin receptor Tie-2 is expressed exclusively in endothelial cells and promotes anigiogenesis [44,45].…”

Section: Discussionmentioning

confidence: 99%

Effects of plant lectin and extracts on adhesion molecules of endothelial progenitors

Iordache¹,

Iordache²,

et al. 2011

Open Life Sciences

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Promise of cell therapy has advanced the use of adult stem cells towards the development of novel approaches to promote regeneration of injured endothelium. The aim of this study was to stimulate endothelial progenitor cells (EPCs) with lectin isolated from Solanum tuberosum (potato) shoot and Calendula officinalis (marigold) extracts, in order to increase EPCs proliferation and gene expression of molecules with roles in chemotaxis and adhesion for a better attachment to injured vascular tissue. EPCs were differentiated from umbilical cord blood-derived mononuclear cells and characterized by light microscopy, flow cytometry, and vascular tube-like structures formation on Matrigel. Cell proliferation was determined by MTS assay, and gene expression of molecules involved in EPCs adhesion (VCAM-1, VE-cadherin, ICAM-1, PECAM-1, P-selectin) and chemotaxis was determined (CXCR4, Tie-2) by RT-PCR. For the assessment of cell motility, wound-healing assay was employed. Both potato shoot lectin and marigold extracts stimulated EPCs proliferation in a concentration dependent manner and were able to increase expression of adhesion and chemotactic molecules. Marigold flower extract proved to be more efficient. This study demonstrates the usefulness of potato lectin and marigold extracts to increase EPCs proliferation and modulate gene expression of chemotactic and adhesion molecules, which may facilitate EPCs attachment to injured endothelium.

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Coronary endothelial P-selectin in pathogenesis of myocardial ischemia-reperfusion injury

Cited by 54 publications

References 32 publications

The immune system and cardiac repair

The immune system and cardiac repair

Blockade of the natriuretic peptide receptor guanylyl cyclase-A inhibits NF-κB activation and alleviates myocardial ischemia/reperfusion injury

Effects of plant lectin and extracts on adhesion molecules of endothelial progenitors

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