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Plasma Membrane-derived Extracellular Vesicles (PMEVs) are membrane-coated vesicles of diameter 0.1 to 1.5µm, carrying various proteins inherent in their parental cells. PMEVs are released when cells undergo activation/apoptosis via blebbing and shedding and have a function in intercellular communication. Exposition of phosphatidylserine (PS) on the outer membrane leaflet that mark them as a biologically distinct entity could also explain a role for PMEVs in phagocytosis and thrombosis. The purpose of this review is to outline and discuss some of the functions of PMEVs in detail to throw more light on its biological effects as more research delve into emerging therapies targeting the microvesicle communication system. The role of PMEVs as a differentiation agent and therefore its possible use in differentiation therapy is discussed. In some experiments, the myeloid differentiating agents all trans retinoic acid (ATRA), phorbol 12-myristate 13-acetate (PMA) and histamine, which inhibit promonocyte proliferation, induced an intracellular Ca2+-mediated PMEV release from HL-60 promonocytes. These PMEVs caused HL-60 cells to enter G0/G1 cell cycle arrest and induce terminal monocyte-to-macrophage differentiation through TGF-β1 mediation. The review also discusses the relationship between PMEVs and diseases where it is known that patients with certain inflammatory diseases show increased PMEV levels in the plasma. The review conclude on the fact that PMEVs have a lot of biological functions that are beneficial to the physiological functions in humans and therefore more work is required to elucidate their composition and the mechanisms involved in exertion of their effects.
This study contributes to the existing literature by addressing some aspects of extracellular vesicle release as well as their functions. The topic is of general interest and will be beneficial to potential readers who would want to clarify types of plasma extracellular vesicles, their functions or pathological effects.
Impaired Immune Phenotype of Circulating Endothelial-Derived Microparticles in None-Diabetic Patients with Chronic Heart Failure: Impact on Insulin Resistance
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Alexander E. Berezin , Alexander A. Kremzer , Tatyana A Samura , Tatyana A Berezina (2015). Impaired Immune Phenotype of Circulating Endothelial-Derived Microparticles in None-Diabetic Patients with Chronic Heart Failure: Impact on Insulin Resistance. Journal of Cells, 1(2): 20-32. DOI: 10.18488/journal.97/2015.1.2/126.96.36.199
Background: The causality role of different immune phenotype in IR developing among chronic heart failure (CHF) subjects has not determined obviously. The aim of the study was to assess relationship between IR and immune phenotype of circulating endothelial-derived microparticles (EMPs) in patients with CHF. Methods: The study retrospectively involved 300 CHF patients aged 48 to 62 years. All the patients have given written informed consent for participation in the study. Biomarkers were measured at baseline of the study. Results: These were not significant differences between both cohort patients in EMPs labeled as CD144+/CD31+, CD144+/annexin V+, and CD62E+ microparticles. Higher concentrations of CD144+/CD31+/annexin V+ EMPs and CD31+/annexin V+ EMPs were found in IR subjects when compared with none IR patients. Using multivariate logistic regression analyses, we found that HOMA-IR (OR = 1.14, 95% CI=1.08-1.21, P = 0.001), NT-proBNP (OR = 1.07, 95% CI=1.04-1.10, P = 0.001), hs-CRP (OR = 1.04, 95% CI=1.02-1.07, P = 0.001), and NYHA class (OR = 1.03, 95% CI=1.01-1.05, P = 0.001) were predictors for increased CD31+/annexin V+ EMPs. Therefore, HOMA-IR (OR = 1.10, 95% CI=1.05-1.17, P = 0.001), NT-proBNP (OR = 1.08, 95% CI=1.04-1.12, P = 0.001), and NYHA class (OR = 1.05, 95% CI=1.02-1.09, P = 0.001) significantly predicted elevation of CD144+/CD31+/annexin V+ EMPs. Conclusion: we found that IR remains statistically significant predictor for increased apoptotic-derived EMPs labelled as CD144+/CD31+/annexin V+ and CD31+/annexin V+ EMPsin none-diabetic patients with CHF patients and that these findings reflect exiting impaired phenotype of circulating EMPs in this patient population.
The paper’s primary contribution is finding that insulin resistance may predict being of impaired phenotype of circulating endothelial-derived microparticles among none-diabetic patients with chronic heart failure.