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Showing 1001–1020 of 2058 publications.
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Di Bartolo, Belinda Ann; Kavurma, Mary M.Receptor activator of nuclear factor-?B ligand (RANKL) is a member of the tumour necrosis factor family important in bone remodelling. Recent evidence suggest that calcification in the vessel wall is equivalent to mechanisms mediating bone formation. This review highlights the role of RANKL in vascular arterial calcification. Here, the relationship between RANKL, osteoprotegerin (OPG) and tumour necrosis factor-related apoptosis-inducing ligand (TRAIL) is discussed. Furthermore, we focus on the regulatory mechanisms mediating RANKL gene expression and transcription in cells of the vessel wall. A better understanding of RANKL-mediated signalling may help develop more sophisticated cell-based therapies to inhibit calcification of the vessel wall. 2014 Bentham Science Publishers.
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Hawkins, Clare L.; Davies, Michael J.Background: Electron paramagnetic resonance (EPR) spectroscopy (also known as electron spin resonance, ESR, spectroscopy) is widely considered to be the "gold standard" for the detection and characterisation of radicals in biological systems. Scope of review: The article reviews the major positive and negative aspects of EPR spectroscopy and discusses how this technique and associated methodologies can be used to maximise useful information, and minimise artefacts, when used in biological studies. Consideration is given to the direct detection of radicals (at both ambient and low temperature), the use of spin trapping and spin scavenging (e.g. reaction with hydroxylamines), the detection of nitric oxide and the detection and quantification of some transition metal ions (particularly iron and copper) and their environment. Major conclusions: When used with care this technique can provide a wealth of valuable information on the presence of radicals and some transition metal ions in biological systems. It can provide definitive information on the identity of the species present and also information on their concentration, structure, mobility and interactions. It is however a technique that has major limitations and the user needs to understand the various pitfalls and shortcoming of the method to avoid making errors. General significance: EPR remains the most definitive method of identifying radicals in complex systems and is also a valuable method of examining radical kinetics, concentrations and structure. This article is part of a Special Issue entitled Current methods to study reactive oxygen species - pros and cons and biophysics of membrane proteins. Guest Editor: Christine Winterbourn. 2013 Elsevier B.V. All rights reserved.
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Brown, Bronwyn E.; Kim, Christine H.J.; Torpy, Fraser R.; Bursill, C. A.; McRobb, Lucinda S.; Heather, Alison Kay; Davies, Michael J.; Van Reyk, David M.Objective: Carnosine has been shown to modulate triglyceride and glycation levels in cell and animal systems. In this study we investigated whether prolonged supplementation with carnosine inhibits atherosclerosis and markers of lesion stability in hyperglycaemic and hyperlipidaemic mice. Methods: Streptozotocin-induced diabetic apo E-/- mice were maintained for 20 weeks, post-induction of diabetes. Half of the animals received carnosine (2g/L) in their drinking water. Diabetes was confirmed by significant increases in blood glucose and glycated haemoglobin, plasma triglyceride and total cholesterol levels, brachiocephalic artery and aortic sinus plaque area; and lower body mass. Results: Prolonged carnosine supplementation resulted in a significant (~20-fold) increase in plasma carnosine levels, and a significant (~23%) lowering of triglyceride levels in the carnosine-supplemented groups regardless of glycaemic status. Supplementation did not affect glycaemic status, blood cholesterol levels or loss of body mass. In the diabetic mice, carnosine supplementation did not diminish measured plaque area, but reduced the area of plaque occupied by extracellular lipid (~60%) and increased both macrophage numbers (~70%) and plaque collagen content (~50%). The area occupied by ?-actin-positive smooth muscle cells was not significantly increased. Conclusions: These data indicate that in a well-established model of diabetes-associated atherosclerosis, prolonged carnosine supplementation enhances plasma levels, and has novel and significant effects on atherosclerotic lesion lipid, collagen and macrophage levels. These data are consistent with greater lesion stability, a key goal in treatment of existing cardiovascular disease. Carnosine supplementation may therefore be of benefit in lowering triglyceride levels and suppressing plaque instability in diabetes-associated atherosclerosis. 2013 Elsevier Ireland Ltd.
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Dunn, Louise L.; Simpson, Philippa J.L.; Prosser, Hamish C.G.; Lecce, Laura; Yuen, Gloria S.C.; Buckle, Andrew M.; Sieveking, Daniel P.; Vanags, Laura Z.; Lim, Patrick R.; Chow, Renee W.Y.; Lam, Yuen Ting; Clayton, Zoe E.; Bao, Shishan San; Davies, Michael J.; Stadler, Nadina; Celermajer, David S.; Stocker, Roland; Bursill, C. A.; Cooke, John P.; Ng, Martin K.C.Impaired angiogenesis in ischemic tissue is a hallmark of diabetes. Thioredoxin-interacting protein (TXNIP) is an exquisitely glucose-sensitive gene that is overexpressed in diabetes. As TXNIP modulates the activity of the key angiogenic cytokine vascular endothelial growth factor (VEGF), we hypothesized that hyperglycemia-induced dysregulation of TXNIP may play a role in the pathogenesis of impaired angiogenesis in diabetes. In the current study, we report that high glucose- mediated overexpression of TXNIP induces a widespread impairment in endothelial cell (EC) function and survival by reducing VEGF production and sensitivity to VEGF action, findings that are rescued by silencing TXNIP with small interfering RNA. High glucose-induced EC dysfunction was recapitulated in normal glucose conditions by overexpressing either TXNIP or a TXNIP C247S mutant unable to bind thioredoxin, suggesting that TXNIP effects are largely independent of thioredoxin activity. In streptozotocin-induced diabetic mice, TXNIP knockdown to nondiabetic levels rescued diabetes-related impairment of angiogenesis, arteriogenesis, blood flow, and functional recovery in an ischemic hindlimb. These findings were associated with in vivo restoration of VEGF production to nondiabetic levels. These data implicate a critical role for TXNIP in diabetes-related impairment of ischemia-mediated angiogenesis and identify TXNIP as a potential therapeutic target for the vascular complications of diabetes. 2014 by the American Diabetes Association.
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Iyengar, Ajay J.; Winlaw, David S.; Galati, John C.; Gentles, Thomas L.; Weintraub, Robert G.; Justo, Robert N.; Wheaton, Gavin R.; Bullock, Andrew M.; Celermajer, David S.; d'Udekem, Yves A.Background: The Fontan procedure is the final in a series of staged palliations for single-ventricle congenital heart disease, which encompasses rare and heterogeneous cardiac lesions. It represents an unusual and novel physiological state characterised by absence of a subpulmonary ventricle. Aims: The population is growing steadily, prompting creation of this registry to study their epidemiology, demographic trends, treatment and outcomes. Methods: This multicentre, binational, prospective and retrospective, web-based registry involving all congenital cardiac centres in the region has identified nearly all Fontan patients in Australia and New Zealand. Patients identified retrospectively were approached for recruitment. New recipients are automatically enrolled prospectively unless they choose to opt-out. Follow-up data are collected yearly. Results: Baseline data were obtained in 1072 patients as at 1 January 2011. Ninety-nine patients died; 64 were lost to follow up. Forty-four per cent of patients lost were between 20 and 30 years of age. The size of the Fontan population is increasing steadily. Among 973 living patients, 541 (56%) gave consent for prospective collection of follow up. Between 1 January 2011 and 1 January 2013, an additional 47 subjects were enrolled prospectively. The current proportion of patients operated with hypoplastic left heart syndrome is currently 29% and is growing rapidly. Conclusion: The population surviving after the Fontan procedure has been growing in recent decades, especially since survival with hypoplastic left heart syndrome has improved. The Australia and New Zealand Fontan Registry provides population-based data, and only large databases like this will give opportunities for understanding the population and performing prospective trials. 2013 Royal Australasian College of Physicians.
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Gray, Belinda R.; Spies, Judith M.; Ng, Martin K.C.[No abstract available]
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Hughan, Sascha C.; Spring, Christopher M.; Schoenwaelder, Simone M.; Sturgeon, Sharelle A.; Alwis, Imala D.; Yuan, Yuping; McFadyen, James D.; Westein, Erik; Goddard, Duncan; Ono, Akiko; Yamanashi, Yuji; Nesbitt, Warwick S.; Jackson, Shaun P.Background: Dok proteins are negative regulators of immunoreceptor signaling and, potentially, integrin adhesion receptors. Results: Deficiency of Dok-2 results in enhanced shear-dependent integrin adhesion in platelets, leading to accelerated platelet thrombus growth. Conclusion: Dok-2 is a shear-specific negative regulator of blood clot formation. Significance: Dok-2 regulates biomechanical platelet adhesion, and targeting this molecule may provide new avenues to regulate thrombosis. 2014 by The American Society for Biochemistry and Molecular Biology, Inc.
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Tabet, Fatiha; Vickers, Kasey C.; Cuesta Torres, Luisa F.; Wiese, Carrie B.; Shoucri, Bassem M.; Lambert, Gilles; Catherinet, Claire; Prado-Louren, Leonel; Levin, Michael G.; Thacker, Seth G.; Sethupathy, Praveen; Barter, Philip J.; Remaley, Alan Thomas; Rye, Kerry AnneHigh-density lipoproteins (HDL) have many biological functions, including reducing endothelial activation and adhesion molecule expression. We recently reported that HDL transport and deliver functional microRNAs (miRNA). Here we show that HDL suppresses expression of intercellular adhesion molecule 1 (ICAM-1) through the transfer of miR-223 to endothelial cells. After incubation of endothelial cells with HDL, mature miR-223 levels are significantly increased in endothelial cells and decreased on HDL. However, miR-223 is not transcribed in endothelial cells and is not increased in cells treated with HDL from miR-223 -/- mice. HDL inhibit ICAM-1 protein levels, but not in cells pretreated with miR-223 inhibitors. ICAM-1 is a direct target of HDL-transferred miR-223 and this is the first example of an extracellular miRNA regulating gene expression in cells where it is not transcribed. Collectively, we demonstrate that HDL's anti-inflammatory properties are conferred, in part, through HDL-miR-223 delivery and translational repression of ICAM-1 in endothelial cells. 2014 Macmillan Publishers Limited.
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Wu, Ben Jing; Ong, Kwok Leung; Shrestha, Sudichhya; Chen, Kang; Tabet, Fatiha; Barter, Philip J.; Rye, Kerry AnneOBJECTIVE - : This study questions whether high-density lipoproteins (HDLs) and apolipoprotein A-I inhibit joint inflammation in streptococcal cell wall peptidoglycan-polysaccharide (PG-PS)-induced arthritis in female Lewis rats. APPROACH AND RESULTS - : Administration of PG-PS to female Lewis rats caused acute joint inflammation after 4 days, followed by remission by day 8. The animals subsequently developed chronic joint inflammation that persisted until euthanasia at day 21. Treatment with apolipoprotein A-I 24 hours before and 24 hours after PG-PS administration reduced the acute and chronic joint inflammation. Treatment with apolipoprotein A-I at days 7, 9, and 11 after PG-PS administration reduced the chronic joint inflammation. Treatment with apolipoprotein A-I or reconstituted HDLs consisting of apolipoprotein A-I complexed with phosphatidylcholine 24 hours before and at days 1, 7, 9, and 11 after PG-PS administration reduced acute and chronic joint inflammation. Treatment with apolipoprotein A-I also reduced the inflammatory white blood cell count, synovial fluid proinflammatory cytokine levels, synovial tissue macrophage accumulation, as well as toll-like receptor 2, and inflammatory cytokine expression. At the molecular level, preincubation of human monocyte-derived macrophages with apolipoprotein A-I or reconstituted HDLs before PG-PS stimulation inhibited the PG-PS-induced increase in toll-like receptor 2 and myeloid differentiation primary response gene (88) mRNA levels, nuclear factor-?B activation, and proinflammatory cytokine production. The effects of apolipoprotein A-I and reconstituted HDLs were abolished by transfecting the human monocyte-derived macrophages with ATP-binding cassette transporter A1 or G1 siRNA. CONCLUSIONS - : Apolipoprotein A-I and reconstituted HDLs attenuate PG-PS-induced arthritis in the rat. Studies in human monocyte-derived macrophages indicate that this benefit may be because of the inhibition of toll-like receptor 2 expression and decreased nuclear factor-?B activation in macrophages. 2013 American Heart Association, Inc.
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Charlton, Francesca; Tooher, Jane M.; Rye, Kerry Anne; Hennessy, AnnemarieIt has been widely thought that the effects of hypertension in pregnancy reversed after delivery and hypertension values returned to their pre-pregnancy level as it was seen as a disease of short duration in otherwise healthy young women. However, recent studies have demonstrated that the principal underlying abnormality, endothelial dysfunction, remains in women who had preeclampsia and that it is this damage that increases the risk of developing cardiovascular disease (CVD) in later life. The contributions of hypertension and dyslipidaemia before and during the pregnancy are also important and contribute to future risk. Serum lipids are complex and change dramatically in pregnancy. In general there is an increase in most plasma lipid components, notably triglycerides, total cholesterol and the major particles of HDL and LDL. Aberrations or exaggerations in this shift (i.e. decrease HDL and a greater increase in LDL) are associated with poor outcomes of pregnancy such as preeclampsia. Long term cardiovascular disease is influenced by preeclampsia and in part potentially by the lipid changes which escalate late in disease. Whether we can influence the risk of preeclampsia by controlling cardiovascular risk factors preceding or during preeclampsia, or cardiovascular disease after preeclampsia is yet to be determined. Ultimately, strategies to control lipid concentrations will only be viable when we understand the safety to the mother at the time of the pregnancy, and to the foetus both immediately and in the very long term. Strategies to control blood pressure are well established in the non-pregnant population, and previous preeclampsia and gestational hypertension should be considered in any cardiovascular risk profile. Whether control of blood pressure in the pregnancy per se is of any longer term benefit is also yet to be determined. 2013.
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Storkey, Corin M.; Pattison, David I.; Gaspard, Dan S.; Hagestuen, Erik D.; Davies, Michael J.The sodium, potassium, or mixed sodium/potassium salt of the naturally occurring high-potency sweetener (2R,4R)-monatin, also known by the common name arruva, degrades over time in model beverage solutions in the presence of light. By use of UHPLC, LC-MS/MS, and peroxide assays, it has been demonstrated that degradation is accelerated by UV/visible light and the presence of trace metal ions. Data are presented that are consistent with a role for singlet oxygen (1O<inf>2</inf>), free radicals, and peroxides (both H <inf>2</inf>O<inf>2</inf> and organic peroxides) in monatin oxidation. Separation of degradation products by UHPLC/HPLC or LC-MS/MS provided evidence for the formation of hydroxylated and peroxide species formed on the indole ring (mass increases 16 and 32, respectively) as well as multiple ring and side-chain oxidation and scission products. Model oxidation systems using the photosensitizer Rose Bengal as a source of 1O<inf>2</inf> support the proposed photodegradation pathways. 2014 American Chemical Society.
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Jeewandara, Thamarasee M.; Wise, Steven G.; Ng, Martin K.C.Cardiovascular disease is the dominant cause of mortality in developed countries, with coronary artery disease (CAD) a predominant contributor. The development of stents to treat CAD was a significant innovation, facilitating effective percutaneous coronary revascularization. Coronary stents have evolved from bare metal compositions, to incorporate advances in pharmacological therapy in what are now known as drug eluting stents (DES). Deployment of a stent overcomes some limitations of balloon angioplasty alone, but provides an acute stimulus for thrombus formation and promotes neointimal hyperplasia. First generation DES effectively reduced in-stent restenosis, but profoundly delay healing and are susceptible to late stent thrombosis, leading to significant clinical complications in the long term. This review characterizes the development of coronary stents, detailing the incremental improvements, which aim to attenuate the major clinical complications of thrombosis and restenosis. Despite these enhancements, coronary stents remain fundamentally incompatible with the vasculature, an issue which has largely gone unaddressed. We highlight the latest modifications and research directions that promise to more holistically design coronary implants that are truly biocompatible. 2014 by the authors.
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Lalley, Peter M.; Pilowsky, Paul M.; Forster, Hubert V.; Zuperku, Edward J.[No abstract available]
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Lalley, Peter M.; Pilowsky, Paul M.; Forster, Hubert V.; Zuperku, Edward J.[No abstract available]
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Surmon, Laura; Bobek, Gabriele; Makris, Angela; Chiu, Christine L.; Lind, Craig A.; Lind, Joanne Maree; Hennessy, AnnemarieBackground: Preeclampsia is a complication of pregnancy characterised by gestational hypertension and proteinuria and is a leading cause of morbidity and mortality in both mothers and infants. Certain anti-angiogenic factors have long been implicated in the pathogenesis of preeclampsia and the placental expression of factors such as soluble fms-like tyrosine kinase-1 (sFLT-1) are often reported in studies of normal and diseased placentae. Despite evidence showing significant differences in placental gene expression by collection site, many studies fail to provide sufficient details on sample selection and collection. Findings. With ourselves and others investigating and reporting on the expression of FLT-1 variants and other genes in the placenta of normotensive and preeclamptic patients, we felt it prudent to examine the variation in expression of FLT-1 variants across human placenta. We examined the differential expression of FLT-1 variants in samples obtained from 12 sites on normal and preeclamptic placentae and found expression to be highly variable between sites. We therefore developed an algorithim to calculate the mean expression for any number of these sites collected and in any combination. The coefficient of variation for all combinations of sites was then used to determine the minimum number of sites required to reduce coefficient of variation to below an acceptable 10%. We found that 10 and 11 sites had to be sampled in the normal and preeclamptic placentae respectively to ensure a representative expression pattern for all FLT-1 variants for an individual placenta. Conclusions: These findings demonstrate significant variation in expression levels of several commonly investigated genes across sites in both normal and preeclamptic placenta. This highlights both the importance of adequate sampling of human placenta for expression studies and the effective communication of sample selection and collection methods, for data interpretation and to ensure the reproducibility and reliability of results and conclusions drawn. 2014 Surmon et al.; licensee BioMed Central Ltd.
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Cartland, Si; Erlich, Jonathan H.; Kavurma, Mary M.Background: We recently demonstrated that TNF-related apoptosis-inducing ligand (TRAIL) is protective of diet-induced diabetes in mice. While TRAIL has been implicated in chronic kidney disease, its role in vivo in diabetic nephropathy is not clear. The present study investigated the role of TRAIL in the pathogenesis of diabetic nephropathy using TRAIL-/-ApoE -/- mice. Methods: TRAIL-/-ApoE-/- and ApoE-/- mice were fed a high fat diet for 20 w. Plasma glucose and insulin levels were assessed over 0, 5, 8 and 20 w. At 20 w, markers of kidney function including creatinine, phosphate, calcium and cystatin C were measured. Changes in mRNA expression of MMPs, TIMP-1, IL-1? and IL-18 were assessed in the kidney. Functional and histological changes in kidneys were examined. Glucose and insulin tolerance tests were performed. Results: TRAIL -/-ApoE-/- mice had significantly increased urine protein, urine protein:creatinine ratio, plasma phosphorous, and plasma cystatin C, with accelerated nephropathy. Histologically, increased extracellular matrix, mesangial expansion and mesangial cell proliferation in the glomeruli were observed. Moreover, TRAIL-/-ApoE-/- kidneys displayed loss of the brush border and disorganisation of tubular epithelium, with increased fibrosis. TRAIL-deficient kidneys also had increased expression of MMPs, TIMP-1, PAI-1, IL-1? and IL-18, markers of renal injury and inflammation. Compared with ApoE-/- mice, TRAIL-/-ApoE-/- mice displayed insulin resistance and type-2 diabetic features with reduced renal insulin-receptor expression. Conclusions: Here, we show that TRAIL-deficiency in ApoE-/- mice exacerbates nephropathy and insulin resistance. Understanding TRAIL signalling in kidney disease and diabetes, may therefore lead to novel strategies for the treatment of diabetic nephropathy. 2014 Cartland et al.
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Hajian, Hamid; Wise, Steven G.; Bax, Daniel V.; Kondyurin, Alexey V.; Waterhouse, Anna; Dunn, Louise L.; Kielty, Cay M.; Yu, Young; Weiss, Anthony Steven; Bilek, Marcela M.M.; Bannon, Paul Gerard; Ng, Martin K.C.Current vascular biomaterials exhibit poor biocompatibility characterised by failure to promote endothelialisation, predisposition to neoinitmal hyperplasia and excessive thrombogenicity. Fibrillin-1, a major constituent of microfibrils is associated with elastic fibres in the arterial wall. Fibrillin-1 binds to endothelial cells through an RGD cell adhesion motif in the fourth TB module. The RGD motif is present in PF8, a recombinant fibrillin-1 fragment. We investigated the potential of PF8 to improve the biocompatibility of PTFE. PF8 enhanced endothelial cell attachment and cell proliferation to a greater extent than fibronectin (p< 0.01). PF8 immobilised on PTFE using plasma immersion ion implantation (PIII), retained these favourable cell interactive properties, again promoting endothelial cell attachment and proliferation. The thrombogenicity of covalently bound PF8 on PTFE was assessed in both static and dynamic conditions. In static conditions, uncoated PIII treated PTFE was more thrombogenic than untreated PTFE, while PF8 coating reduced thrombogenicity. Under flow, there was no difference in the thrombogenicity of PF8 coated PTFE and untreated PTFE. Immobilised PF8 shows a striking ability to promote attachment and growth of endothelial cells on PTFE, while providing a non-thrombogenic surface. These features make PF8 a promising candidate to improve the biocompatibility of current synthetic vascular grafts. 2014.
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Thompson, Peter Lindsay[No abstract available]
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Chuang, Christine Y.; Degendorfer, Georg; Hammer, Astrid; Whitelock, John; Malle, Ernst; Davies, Michael J.ECM (extracellular matrix) materials, such as laminin, perlecan, type IV collagen and fibronectin, play a key role in determining the structure of the arterial wall and the properties of cells that interact with the ECM. The aim of the present study was to investigate the effect of peroxynitrous acid, an oxidant generated by activated macrophages, on the structure and function of the ECM laid down by HCAECs (human coronary artery endothelial cells) in vitro and in vivo. We show that exposure of HCAEC-derived native matrix components to peroxynitrous acid (but not decomposed oxidant) at concentrations >1 ?M results in a loss of antibody recognition of perlecan, collagen IV, and cell-binding sites on laminin and fibronectin. Loss of recognition was accompanied by decreased HCAEC adhesion. Real-time PCR showed up-regulation of inflammation-associated genes, including MMP7 (matrix metalloproteinase 7) and MMP13, as well as down-regulation of the laminin ? 2 chain, in HCAECs cultured on peroxynitrous acid-treated matrix compared with native matrix. Immunohistochemical studies provided evidence of co-localization of laminin with 3-nitrotyrosine, a biomarker of peroxynitrous acid damage, in type II-III/IV human atherosclerotic lesions, consistent with matrix damage occurring during disease development in vivo. The results of the present study suggest a mechanism through which peroxynitrous acid modifies endothelial cell-derived native ECM proteins of the arterial basement membrane in atherosclerotic lesions. These changes to ECM and particularly perlecan and laminin may be important in inducing cellular dysfunction and contribute to atherogenesis. The Authors Journal compilation 2014 Biochemical Society.
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Chan, Kim Hoe; Simpson, Philippa J.L.; Yong, Andy Sze Chiang; Dunn, Louise L.; Chawantanpipat, Chirapan; Hsu, Chijen; Yu, Young; Keech, Anthony C.; Celermajer, David S.; Ng, Martin K.C.Background: Endothelial progenitor cells (EPCs) are implicated in protection against vascular disease. However, studies using angiography alone have reported conflicting results when relating EPCs to epicardial coronary artery disease (CAD) severity. Moreover, the relationship between different EPC types and the coronary microcirculation is unknown. We therefore investigated the relationship between EPC populations and coronary epicardial and microvascular disease. Methods: Thirty-three patients with a spectrum of isolated left anterior descending artery disease were studied. The coronary epicardial and microcirculation were physiologically interrogated by measurement of fractional flow reserve (FFR), index of microvascular resistance (IMR) and coronary flow reserve (CFR). Two distinct EPC populations (early EPC and late outgrowth endothelial cells [OECs]) were isolated from these patients and studied ex vivo. Results: There was a significant inverse relationship between circulating OEC levels and epicardial CAD severity, as assessed by FFR and angiography (r = 0.371, p = 0.04; r = -0.358, p = 0.04; respectively). More severe epicardial CAD was associated with impaired OEC migration and tubulogenesis (r = 0.59, p = 0.005; r = 0.589, p = 0.004; respectively). Patients with significant epicardial CAD (FFR,0.75) had lower OEC levels and function compared to those without hemodynamically significant stenoses (p,0.05). In contrast, no such relationship was seen for early EPC number and function, nor was there a relationship between IMR and EPCs. There was a significant relationship between CFR and OEC function. Conclusions: EPC populations differ in regards to their associations with CAD severity. The number and function of OECs, but not early EPCs, correlated significantly with epicardial CAD severity. There was no relationship between EPCs and severity of coronary microvascular disease.
