• Corpus ID: 81142555

Studies on the role of GPR55 in cardiovascular physiology and pathophysiology

  title={Studies on the role of GPR55 in cardiovascular physiology and pathophysiology},
  author={Olivia Jane Robertson-Gray},
Atherosclerosis is a multifactorial, chronic inflammatory condition characterised by endothelial dysfunction, hyperlipidaemia and the accumulation of fatty deposits within the tunica intima of medium-to-large sized muscular arteries. [] Key Result Using C57BL/6 (wildtype; WT), apolipoprotein E knockout (ApoE-/-; mouse model of atherosclerosis), GPR55 knockout (GPR55-/-) and novel ApoE-/-/GPR55-/- mice, this study has established that in the presence of high fat feeding (to accelerate atherosclerosis), GPR55…


Animal Models of Atherosclerosis
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Consumption of a high-cholesterol diet results in lumen obstructive plaque formation in ApoE(-/-) mice, which significantly alters aortic root haemodynamics, associated with impaired NO-dependent vasodilation in vessel segments known to be prone to atherosclerosis.
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Findings point to GPR55 as a novel G protein-coupled receptor regulating cardiac function at two cellular sites, and the first evidence that, in cultured neonatal ventricular myocytes, LPI triggers distinct signaling pathways via GPR 55, depending on receptor localization is provided.
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Protective Effects of PARP-1 Knockout on Dyslipidemia-Induced Autonomic and Vascular Dysfunction in ApoE−/− Mice: Effects on eNOS and Oxidative Stress
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Treatment with the GPR55 antagonist CID16020046 increases neutrophil activation in mouse atherogenesis.
Results indicate that GPR55 is critical for the negative control of neutrophil activation in different phases of atherogenesis, and increased levels of the endocannabinoid and putative GPR 55 ligand anandamide (AEA) were found, suggesting its possible autocrine control of Neutrophil activity.
Hypercholesterolemia Impairs Endothelium-Dependent Relaxations in Common Carotid Arteries of Apolipoprotein E-Deficient Mice
Increased superoxide anion production in endothelial cells appears to be coupled to activation of cholinergic receptors and is responsible for hypercholesterolemia-induced endothelial dysfunction in apoE-deficient mice.