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Increased Circulating Microparticles in Diabetic Rats Mediate Leukocyte Adhesion in Intact Venules
Author(s) -
Stork Christian,
He Pingnian
Publication year - 2012
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.26.1_supplement.855.1
Subject(s) - microvessel , chemistry , flow cytometry , extravasation , annexin , phosphatidylserine , apoptosis , percoll , streptozotocin , venule , endothelium , pathology , immunology , endocrinology , medicine , centrifugation , diabetes mellitus , angiogenesis , membrane , biochemistry , phospholipid
Microparticles (MPs) are membrane bound vesicles that express phosphatidylserine and released by activated and apoptotic cells. MP amount increases under inflammatory conditions. The objective of this study is to investigate if streptozotocin‐induced diabetic rats had increased circulating MPs and the roles of MPs in development of diabetic microvascular complications. Plasma MPs were quantified by flow cytometry with Annexin‐V staining and isolated by centrifugation. MP interaction with endothelium and blood cells was investigated by perfusing isolated MPs to individually perfused rat mesenteric microvessels and observed by confocal imaging. The diabetic plasma MP count significantly increased from 5.3 × 10 6 (normal rats) to 33 × 10 6 per ml. Perfusing isolated diabetic MPs to the normal venule resulted in rapid MP adhesion on the microvessel wall, which induced immediate leukocyte adhesion following resumed blood flow (19 leukocytes/100 μm vessel length). Although MP‐mediated leukocyte adhesion did not affect basal permeability, the application of a chemoattractant fMLP caused a 5‐fold increase in Lp. These results indicate that the increased circulating MPs under diabetic conditions are not only results of vascular cell activation and apoptosis, but also mediators that promote blood cell adhesion and activation resulting in exacerbated microvessel dysfunction. Supported by HL56237 and HL084338.