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1.
Org Biomol Chem ; 13(45): 11026-38, 2015 Dec 07.
Article in English | MEDLINE | ID: mdl-26393412

ABSTRACT

A systematic investigation of the influence of substitution at positions C-2 and C-3 on the azulenone skeleton, based on NMR characterisation, is discussed with particular focus on the impact of the steric and electronic characteristics of substituents on the position of the norcaradiene-cycloheptatriene (NCD-CHT) equilibrium. Variable temperature (VT) NMR studies, undertaken to enable the resolution of signals for the equilibrating valence tautomers revealed, in addition, interesting shifts in the equilibrium.

2.
Atherosclerosis ; 216(1): 74-82, 2011 May.
Article in English | MEDLINE | ID: mdl-21333993

ABSTRACT

OBJECTIVES: We examined the role of C-fms+ cells in response to vascular injury with a focus on the temporal and spatial platelet interactions, monocyte survival and proliferation within the evolving neointimal lesion and monocyte proliferation within the circulation and specified monocyte reservoir sites. Finally, we investigated the therapeutic effect of C-fms kinase inhibition (CFKI) on neointimal hyperplasia post vessel injury. METHODS AND RESULTS: We utilized murine carotid-wire injury, a transgenic C-fms reporting mouse model, confocal microscopy, shear-flow studies, specific C-fms signalling inhibition to determine the activation, mobilization and recruitment of C-fms+ monocytes in the context of early and late vessel remodelling. C-fms+ cells were recruited as early as 4h and accumulated over time in the neointima following injury. Monocyte interaction with platelet thrombus under flow and in vivo, in addition to monocyte mobilisation into the circulation post-injury was impaired by CFKI administration. Sustained inhibition of C-fms over 1-2 weeks abrogated the neointimal response but preserved re-endothelialisation post-injury. CONCLUSION: These data establish C-fms as a key regulator of the vascular response to injury and a potentially attractive therapeutic target in disease states where neointimal hyperplasia, monocyte activation and pathologic remodelling are prominent and endothelial homeostasis is desirable.


Subject(s)
Carotid Arteries/metabolism , Carotid Artery Injuries/metabolism , Monocytes/metabolism , Receptor, Macrophage Colony-Stimulating Factor/metabolism , Tunica Intima/metabolism , Vascular System Injuries/metabolism , Animals , Blood Platelets/metabolism , CD11b Antigen/metabolism , Carotid Arteries/drug effects , Carotid Arteries/pathology , Carotid Artery Injuries/drug therapy , Carotid Artery Injuries/genetics , Carotid Artery Injuries/pathology , Cell Movement , Cell Proliferation , Cell Survival , Cells, Cultured , Disease Models, Animal , Hemorheology , Hyperplasia , Mice , Mice, Inbred C57BL , Mice, Transgenic , Microscopy, Confocal , Monocytes/drug effects , Monocytes/pathology , Platelet Adhesiveness , Protein Kinase Inhibitors/pharmacology , Receptor, Macrophage Colony-Stimulating Factor/genetics , Time Factors , Tunica Intima/drug effects , Tunica Intima/injuries , Tunica Intima/pathology , Vascular System Injuries/drug therapy , Vascular System Injuries/genetics , Vascular System Injuries/pathology
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