Circulating microparticles from diabetic rats impair endothelial function and regulate endothelial protein expression

Diabetes mellitus increases the risk of cardiovascular disease, which is accompanied by functional and structural changes in the vascular system. Microparticles (MPs) have been described as biological vectors of endothelial dysfunction in other pathologies. However, the molecular mechanisms underlying their formation and signalling are unclear. We investigated the role of MPs derived from streptozotocin (STZ)‐induced diabetic rats in endothelial function.

[1]  W. Qu,et al.  Resveratrol Ameliorates High Glucose and High-Fat/Sucrose Diet-Induced Vascular Hyperpermeability Involving Cav-1/eNOS Regulation , 2014, PloS one.

[2]  K. Taguchi,et al.  Activated Platelets from Diabetic Rats Cause Endothelial Dysfunction by Decreasing Akt/Endothelial NO Synthase Signaling Pathway , 2014, PloS one.

[3]  Ying Wang,et al.  Microvesicles and diabetic complications — novel mediators, potential biomarkers and therapeutic targets , 2014, Acta Pharmacologica Sinica.

[4]  S. Faure,et al.  Opposite effects of angiotensins receptors type 2 and type 4 on streptozotocin induced diabetes vascular alterations in mice , 2014, Cardiovascular Diabetology.

[5]  K. Kamata,et al.  Mechanisms underlying reduced P2Y1‐receptor‐mediated relaxation in superior mesenteric arteries from long‐term streptozotocin‐induced diabetic rats , 2013, Acta physiologica.

[6]  K. Kamata,et al.  Suppressed G‐protein‐coupled receptor kinase 2 activity protects female diabetic‐mouse aorta against endothelial dysfunction , 2013, Acta physiologica.

[7]  K. Kamata,et al.  Involvement of CaM kinase II in the impairment of endothelial function and eNOS activity in aortas of Type 2 diabetic rats. , 2012, Clinical science.

[8]  K. Kamata,et al.  G Protein–Coupled Receptor Kinase 2, With β-Arrestin 2, Impairs Insulin-Induced Akt/Endothelial Nitric Oxide Synthase Signaling in ob/ob Mouse Aorta , 2012, Diabetes.

[9]  K. Kamata,et al.  Pravastatin normalizes endothelium‐derived contracting factor‐mediated response via suppression of Rho‐kinase signalling in mesenteric artery from aged type 2 diabetic rat , 2012, Acta physiologica.

[10]  M. Lederman,et al.  Increased Platelet and Microparticle Activation in HIV Infection: Upregulation of P-Selectin and Tissue Factor Expression , 2012, Journal of acquired immune deficiency syndromes.

[11]  K. Kamata,et al.  Mechanisms underlying altered extracellular nucleotide-induced contractions in mesenteric arteries from rats in later-stage type 2 diabetes: effect of ANG II type 1 receptor antagonism. , 2011, American journal of physiology. Heart and circulatory physiology.

[12]  D. Bluemke,et al.  Myocardial Structure, Function, and Scar in Patients With Type 1 Diabetes Mellitus , 2011, Circulation.

[13]  S. Faure,et al.  Paradoxical effects of ethoxidine, a topoisomerase I inhibitor, in the cellular processes leading to angiogenesis on endothelial cells. , 2011, Carcinogenesis.

[14]  W. Wier,et al.  Exercise improves the dilatation function of mesenteric arteries in postmyocardial infarction rats via a PI3K/Akt/eNOS pathway-mediated mechanism. , 2010, American journal of physiology. Heart and circulatory physiology.

[15]  R. Andriantsitohaina,et al.  Circulating microparticles from pulmonary hypertensive rats induce endothelial dysfunction. , 2010, American journal of respiratory and critical care medicine.

[16]  A. Michelson.  Antiplatelet therapies for the treatment of cardiovascular disease , 2010, Nature Reviews Drug Discovery.

[17]  G. Leftheriotis,et al.  Endothelial dysfunction caused by circulating microparticles from patients with metabolic syndrome. , 2008, The American journal of pathology.

[18]  W. Grossman,et al.  Circulating endothelial microparticle levels predict hemodynamic severity of pulmonary hypertension. , 2008, American journal of respiratory and critical care medicine.

[19]  Chun Yang,et al.  Lymphocytic microparticles inhibit angiogenesis by stimulating oxidative stress and negatively regulating VEGF-induced pathways. , 2008, American journal of physiology. Regulatory, integrative and comparative physiology.

[20]  J. Suwaidi,et al.  Endothelial dysfunction in diabetes mellitus , 2007, Vascular health and risk management.

[21]  K. Kamata,et al.  Mechanisms underlying the chronic pioglitazone treatment-induced improvement in the impaired endothelium-dependent relaxation seen in aortas from diabetic rats. , 2007, Free radical biology & medicine.

[22]  J. Freyssinet,et al.  Procoagulant Microparticles: Disrupting the Vascular Homeostasis Equation? , 2006, Arteriosclerosis, thrombosis, and vascular biology.

[23]  K. Kamata,et al.  Enhancement of methoxamine‐induced contractile responses of rat ventricular muscle in streptozotocin‐induced diabetes is associated with α1A adrenoceptor upregulation , 2006, Acta physiologica.

[24]  R. Andriantsitohaina,et al.  Origin and biological significance of shed-membrane microparticles. , 2006, Endocrine, metabolic & immune disorders drug targets.

[25]  M. Matsumura,et al.  Increased levels of platelet-derived microparticles in patients with diabetic retinopathy. , 2005, Diabetes research and clinical practice.

[26]  R. Andriantsitohaina,et al.  Shed membrane microparticles from circulating and vascular cells in regulating vascular function. , 2005, American journal of physiology. Heart and circulatory physiology.

[27]  J. Freyssinet,et al.  Circulating procoagulant microparticles and soluble GPV in myocardial infarction treated by primary percutaneous transluminal coronary angioplasty. A possible role for GPIIb‐IIIa antagonists , 2004, Journal of thrombosis and haemostasis : JTH.

[28]  M. Goligorsky,et al.  Endothelium-derived microparticles impair endothelial function in vitro. , 2004, American journal of physiology. Heart and circulatory physiology.

[29]  R. Andriantsitohaina,et al.  Shed Membrane Particles From T Lymphocytes Impair Endothelial Function and Regulate Endothelial Protein Expression , 2004, Circulation.

[30]  R. Nieuwland,et al.  Microparticles in cardiovascular diseases. , 2003, Cardiovascular research.

[31]  N. Hayashi,et al.  Regulation of endothelial nitric oxide synthase by protein kinase C. , 2003, Journal of biochemistry.

[32]  D. Desprez,et al.  Circulating microparticles: a marker of procoagulant state in normal pregnancy and pregnancy complicated by preeclampsia or intrauterine growth restriction , 2003, Thrombosis and Haemostasis.

[33]  Patrice Darmon,et al.  Type 1 and type 2 diabetic patients display different patterns of cellular microparticles. , 2002, Diabetes.

[34]  T. Iwasaka,et al.  Detection of monocyte-derived microparticles in patients with Type II diabetes mellitus , 2002, Diabetologia.

[35]  M. Nieminen,et al.  For Personal Use. Only Reproduce with Permission from the Lancet Publishing Group , 2022 .

[36]  Vincenza Dolo,et al.  Shedding of the matrix metalloproteinases MMP-2, MMP-9, and MT1-MMP as membrane vesicle-associated components by endothelial cells. , 2002, The American journal of pathology.

[37]  A. Tedgui,et al.  Circulating Microparticles From Patients With Myocardial Infarction Cause Endothelial Dysfunction , 2001, Circulation.

[38]  L. Horstman,et al.  Elevated endothelial microparticles in thrombotic thrombocytopenic purpura: findings from brain and renal microvascular cell culture and patients with active disease , 2001, British journal of haematology.

[39]  K. Kamata,et al.  Mechanisms underlying the chronic pravastatin treatment‐induced improvement in the impaired endothelium‐dependent aortic relaxation seen in streptozotocin‐induced diabetic rats , 2000, British journal of pharmacology.

[40]  H. Brühl,et al.  Transfer of the chemokine receptor CCR5 between cells by membrane-derived microparticles: A mechanism for cellular human immunodeficiency virus 1 infection , 2000, Nature Medicine.

[41]  K. Kamata,et al.  Altered endothelium-dependent and -independent hyperpolarization and endothelium-dependent relaxation in carotid arteries isolated from streptozotocin-induced diabetic rats , 2000, Naunyn-Schmiedeberg's Archives of Pharmacology.

[42]  J. Freyssinet,et al.  Elevated levels of shed membrane microparticles with procoagulant potential in the peripheral circulating blood of patients with acute coronary syndromes. , 2000, Circulation.

[43]  J. Freyssinet,et al.  Shed membrane microparticles with procoagulant potential in human atherosclerotic plaques: a role for apoptosis in plaque thrombogenicity. , 1999, Circulation.

[44]  J. Loscalzo,et al.  Endothelial cells in physiology and in the pathophysiology of vascular disorders. , 1998, Blood.

[45]  K S Sakariassen,et al.  Shear-induced platelet activation and platelet microparticle formation at blood flow conditions as in arteries with a severe stenosis. , 1997, Arteriosclerosis, thrombosis, and vascular biology.

[46]  A. Schroit,et al.  Pathophysiologic implications of membrane phospholipid asymmetry in blood cells. , 1997, Blood.

[47]  Brian K. Kobilka,et al.  Behavioural and cardiovascular effects of disrupting the angiotensin II type-2 receptor gene in mice , 1995, Nature.

[48]  Y. Kaneda,et al.  Gene therapy inhibiting neointimal vascular lesion: in vivo transfer of endothelial cell nitric oxide synthase gene. , 1995, Proceedings of the National Academy of Sciences of the United States of America.

[49]  J. Bloodworth.  Diabetes mellitus and vascular disease. , 1973, Postgraduate medicine.

[50]  M. Cooper,et al.  Mechanisms of diabetic complications. , 2013, Physiological reviews.

[51]  C. Stefanadis,et al.  Diabetes mellitus and vascular endothelial dysfunction: current perspectives. , 2012, Current vascular pharmacology.

[52]  Ming Chen,et al.  Circulating level of microparticles and their correlation with arterial elasticity and endothelium-dependent dilation in patients with type 2 diabetes mellitus. , 2010, Atherosclerosis.

[53]  J. Kvasnička,et al.  Tissue factor, tissue factor pathway inhibitor and cytoadhesive molecules in patients with an acute coronary syndrome. , 2003, Physiological research.

[54]  G. Barsh,et al.  Behavioural and cardiovascular effects of disrupting the angiotensin II type-2 receptor gene in mice , 1996, Nature.

[55]  Von der Leyen.  Gene therapy inhibiting neointimal vascular lesion , 1995 .