Blockade of cell adhesion by a small molecule selectin antagonist attenuates myocardial ischemia/reperfusion injury

Onai, Yasuyuki; Suzuki, Jun–ichi; Nishiwaki, Yasunobu; Gotoh, Ryo; Berens, Kurt L.; Dixon, Richard A. F.; Yoshida, Masayuki; Itoh, Hiroshi; Isobe, Mitsuaki

doi:10.1016/j.ejphar.2003.09.040

Cited by 24 publications

(14 citation statements)

References 37 publications

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“…These have potent in vivo and in vitro activity. For example, oligosaccharides have been shown to inhibit eosinophil and neutrophil adhesion to immobilized platelets (Kim et al, 1998), and the monosaccharide dimer: bimosiamose (TBC1269) decreases reperfusion injury after myocardial infarction in rats (Onai et al, 2003). Although the activity of bimosiamose may also be attributable to antagonism of E-selectin, it has shown promising results during clinical development, having improved skin lesions in psoriasis patients and airway reactivity in mild asthmatics (Beeh et al, 2006;Friedrich et al, 2006).…”

Section: P-selectin Inhibitionmentioning

confidence: 99%

Novel uses for anti‐platelet agents as anti‐inflammatory drugs

Pitchford

2007

British J Pharmacology

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An alteration in the character and function of platelets is manifested in patients with inflammatory diseases, and these alterations have been dissociated from the well‐characterized involvement of platelets in thrombosis and haemostasis. Recent evidence reveals platelet activation is sometimes critical in the development of inflammation. The mechanisms by which platelets participate in inflammation are diverse, and offer numerous opportunities for future drug intervention. There is now acceptance that platelets act as innate inflammatory cells in immune responses, with roles as sentinel cells undergoing surveillance, responding to microbial invasion, orchestrating leukocyte recruitment, and migrating through tissue, causing damage and influencing repair processes in chronic disease. Some of these processes are targeted by drugs that are being developed to target platelet participation in atherosclerosis. The actions of platelets therefore influence the pathogenesis of diverse inflammatory diseases in various body compartments, encompassing parasitic and bacterial infection, allergic inflammation (especially asthma and rhinitis), and non‐atopic inflammatory conditions, for example, chronic obstructive pulmonary disease (COPD), rheumatoid arthritis (RA), inflammatory bowel disease (IBD) and atherosclerosis. This review will first discuss the evidence for platelet activation in these various inflammatory diseases, and secondly discuss the mechanisms by which this pathogenesis occurs and the various anti‐platelet agents which have been developed to combat platelet activation in atherosclerosis and their potential future use for the treatment of other inflammatory diseases.British Journal of Pharmacology (2007) 152, 987–1002; doi:10.1038/sj.bjp.0707364; published online 2 July 2007

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Section: P-selectin Inhibitionmentioning

confidence: 99%

Novel uses for anti‐platelet agents as anti‐inflammatory drugs

Pitchford

2007

British J Pharmacology

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“…The chest wall and the skin were then closed with a 3-0 silk suture. [12][13][14][15][16][17][18] This investigation conforms with the Guide for the Care and Use of Laboratory Animals of Tokyo Medical and Dental University. Animals used in this study were maintained in accordance with the Guide for the Care and Use of Laboratory Animals published by the US National Institute of Health (NIH Publication No.…”

Section: Methodsmentioning

confidence: 99%

“…The area ratio (affected/LV as a percentage) was calculated as described previously. [12][13][14][15][16][17][18] Values for 3 ventricular regions were averaged for each heart, and the mean percentage of affected area for each group was calculated. All data were analyzed in a blind fashion by two independent investigators and averaged.…”

Section: -18)mentioning

confidence: 99%

“…M-mode views were used to measure the LV dimensions according to the American Society for Echocardiography leading edge method. [12][13][14][15][16][17][18] LV end-diastolic dimension (LVDd) and end-systolic dimension (LVDs), and fractional shortening (%FS= [(LVDd−LVDs) / LVDd]×100) were calculated from the M-mode recordings. Measurement of area at risk and infarct size: On day 1 after reperfusion, the anesthetized rats were intubated and thoracotomy was repeated.…”

Section: -18)mentioning

confidence: 99%

“…The hearts were then sliced transversely into 4 slices, and incubated in 2.0% triphenyl tetrazolium chloride (TTC) (Sigma, Tokyo) for 15 minutes at 37°C to verify the viable and necrotic area in the ischemic myocardium (area at risk, AAR) as described earlier. [12][13][14][15][16][17][18] Each slice was weighed and photographed, and the areas of infarction, AAR, and left ventricle were evaluated using computerassisted planimetry (Scion Image β4.0.2) by observers blinded to the treatment protocol. The volumes of each area were determined by the following process: volume of AREA = (A1 × Wt1) + (A2 × Wt2) + (A3 × Wt3) + (A4 × Wt4) where A is the percentage of each area by planimetry from subscripted numbers 1-4 indicating sections and Wt is the weight of the same numbered sections.…”

Section: -18)mentioning

confidence: 99%

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Effects of Pharmacological Suppression of Plasminogen Activator Inhibitor-1 in Myocardial Remodeling After Ischemia Reperfusion Injury

et al. 2011

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SummaryPlasminogen activator inhibitor-1 (PAI-1) contributes to cardiac ventricular remodeling because migration of inflammatory cells and attenuation of extracellular matrix degradation are caused by plasmin and matrix metalloproteinase. However, the roles of PAI-1 in myocardial ischemia reperfusion (I/R) injury and the following inflammatory response have not yet been well elucidated. To clarify the role of PAI-1 in myocardial I/R injury, we used a specific PAI-1 inhibitor (IMD-1622) in a rat model. The left anterior descending coronary artery was ligated and reperfusion was performed by loosening the suture after 30 minutes of arterial occlusion. A single administration of IMD-1622 (20 mg/kg) or vehicle was given intraperitoneally and then the rats were sacrificed on day 1 or day 14 after I/R. Blood pressure, echocardiograms, histopathology, and molecular examination were performed. The examinations revealed that PAI-1 inhibitor showed limited effects on cardiac dysfunction and ventricular remodeling after I/R. We conclude that the pharmacological inhibition of PAI-1 may not affect ventricular remodeling after myocardial I/R injury. (Int Heart J 2011; 52: 388-392)

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Mechanisms of Sepsis-Induced Organ Dysfunction and Recovery

Abraham

Singer²

2007

Update in Intensive Care and Emergency Medicine

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The use of general descriptive names, registered names, trademarks, etc. in this publication does not imply, even in the absence of a specific statement, that such names are exempt from the relevant protective laws and regulations and therefore free for general use.Product liability: The publishers cannot guarantee the accuracy of any information about dosage and application contained in this book. In every individual case the user must check such information by consulting the relevant literature.

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Blockade of cell adhesion by a small molecule selectin antagonist attenuates myocardial ischemia/reperfusion injury

Cited by 24 publications

References 37 publications

Novel uses for anti‐platelet agents as anti‐inflammatory drugs

Novel uses for anti‐platelet agents as anti‐inflammatory drugs

Effects of Pharmacological Suppression of Plasminogen Activator Inhibitor-1 in Myocardial Remodeling After Ischemia Reperfusion Injury

Mechanisms of Sepsis-Induced Organ Dysfunction and Recovery

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