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Soluble P-selectin promotes acute myocardial infarction onset but not severity.

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Soluble P-selectin promotes acute myocardial infarction onset but not severity.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Ning, Wenhu Sun, Guizhi Zhao, Kan Wang, Guoyu Guo, Ling
Description	Author Affiliation: Guo L ( Department of Cardiology, The Fourth Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang 150001, P.R. China.); Sun G ( Department of Cardiology, The Fourth Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang 150001, P.R. China.); Wang G ( Department of Pharmacy, The Fourth Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang 150001, P.R. China.); Ning W ( Department of Emergency, The Fourth Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang 150001, P.R. China.); Zhao K ( Department of Emergency, The Fourth Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang 150001, P.R. China.)
Abstract	Pselectin, an integral membrane glycoprotein of platelets and endothelial cells, and the soluble form of Pselectin are hypothesized to play a role in the initiation of atherosclerosis and acute myocardial infarction (AMI). However, limited data are available with which to evaluate the main role of soluble Pselectin (sPselectin) in the onset or the severity of AMI. In the present study, we investigated 15 patients who suffered from angina, 10 patients who underwent percutaneous coronary intervention (PCI) therapy and 10 patients who underwent thrombolysis therapy, compared with 15 volunteers with no cardiovascular disease. We confirmed that the plasma sPselectin levels were increased in patients with obesity (particularly pericardial obesity) and hyperlipidemia, positively correlated with plasma tumor necrosis factor (TNF) and strongly negatively correlated with adiponectin in all patients regardless of AMI status. Furthermore, sPselectin levels were significantly higher in PCI and thrombolysis patients compared with angina patients and the control cohort. However, we observed that sPselectin levels did not change following PCI and thrombolysis therapy. In addition, there was no correlation between sPselectin levels and the severity of AMI in the cohort which received PCI or thrombolysis therapy. Therefore, we deduced that sPselectin only induced the onset of AMI but did not promote its severity. To confirm this hypothesis, a Pselectin inhibitor was administered to an atherosclerosis formation model, plaque rapture model and neointimal hyperplasia model. We revealed that atherosclerotic plaque formation and rupture, neointimal formation and neointimal bleeding were suppressed by the sPselectin inhibitor. We concluded that sPselectin, induced by systemic inflammation in conditions including obesity and hyperlipidemia, promoted atherosclerotic plaque and neointimal formation, plaque rapture and neointimal bleeding, further leading to AMI. We also demonstrated that sPselectin had no effect on the severity of AMI.
ISSN	17912997
e-ISSN	17913004
Journal	Molecular Medicine Reports
Issue Number	3
Volume Number	11
Language	English
Publisher	Spandidos Publications
Publisher Date	2015-03-01
Publisher Place	Greece
Access Restriction	Open
Subject Keyword	Myocardial Infarction Blood P-selectin Animals Atherosclerosis Pathology Chronic Disease Cohort Studies Disease Models, Animal Hyperlipidemias Inflammation Mice, Knockout Diagnosis Genetics Obesity Plaque, Atherosclerotic Risk Factors Severity Of Illness Index Discipline Molecular Biology
Content Type	Text
Resource Type	Article
Subject	Genetics Biochemistry Molecular Biology Cancer Research Molecular Medicine Oncology

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