Research Topics
Genomes and Genes | Christopher L JacksonSummaryAffiliation: University of Bristol Country: UK Publications
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Publications
Animal models of spontaneous plaque rupture: the holy grail of experimental atherosclerosis researchMichael E Rosenfeld
Department of Pathobiology, University of Washington, Box 353410, Seattle 98195, USA
Curr Atheroscler Rep 4:238-42. 2002....
Is there life after plaque rupture?C L Jackson
Bristol Heart Institute, University of Bristol, Level 7, Bristol Royal Infirmary, Bristol BS2 8HW, U K
Biochem Soc Trans 35:887-9. 2007..Interventions that strengthen the plaque, such as pravastatin therapy, do not alter remodelling parameters but instead allow for more outward remodelling before a rupture is caused...
Assessment of unstable atherosclerosis in miceChristopher L Jackson
Bristol Heart Institute, Bristol Royal Infirmary, University of Bristol, Bristol, UK
Arterioscler Thromb Vasc Biol 27:714-20. 2007..These considerations lead us to a number of general recommendations...
Effect of broad-spectrum matrix metalloproteinase inhibition on atherosclerotic plaque stabilityJason L Johnson
Bristol Heart Institute, University of Bristol, Level 7, Bristol Royal Infirmary, Bristol BS2 8HW, United Kingdom
Cardiovasc Res 71:586-95. 2006....
MMP-7 mediates cleavage of N-cadherin and promotes smooth muscle cell apoptosisHelen Williams
Bristol Heart Institute, University of Bristol, Bristol Royal Infirmary, Research Floor Level 7, Upper Maudlin St, Bristol BS2 8HW, UK
Cardiovasc Res 87:137-46. 2010..We previously showed that cell-cell contacts mediated by N-cadherin reduce VSMC apoptosis. This study aimed to determine whether matrix-degrading metalloproteinase (MMP)-dependent N-cadherin cleavage causes VSMC apoptosis...
A selective matrix metalloproteinase-12 inhibitor retards atherosclerotic plaque development in apolipoprotein E-knockout miceJason L Johnson
Bristol Heart Institute, School of Clinical Sciences, University of Bristol, Bristol, United Kingdom
Arterioscler Thromb Vasc Biol 31:528-35. 2011..In this study, we investigated the influence of a greater than 10-fold selective synthetic MMP-12 inhibitor on plaque progression in the apolipoprotein E knockout mouse model of atherosclerosis...
Suppression of atherosclerotic plaque progression and instability by tissue inhibitor of metalloproteinase-2: involvement of macrophage migration and apoptosisJason L Johnson
Bristol Heart Institute, University of Bristol, Bristol, England
Circulation 113:2435-44. 2006..We hypothesized that overexpression of tissue inhibitor of metalloproteinase (TIMP)-1 or TIMP-2 would attenuate atherosclerotic plaque development and instability in high fat-fed apolipoprotein E-knockout (apoE(-/-)) mice...
Destabilizing role of cathepsin S in murine atherosclerotic plaquesKenneth J Rodgers
Bristol Heart Institute, University of Bristol, United Kingdom
Arterioscler Thromb Vasc Biol 26:851-6. 2006..Therefore, we investigated the possibility that the lysosomal proteinase cathepsin S may be involved in atherosclerotic plaque destabilization...
Activation of matrix-degrading metalloproteinases by mast cell proteases in atherosclerotic plaquesJ L Johnson
Bristol Heart Institute, University of Bristol, Bristol Royal Infirmary, Bristol, UK
Arterioscler Thromb Vasc Biol 18:1707-15. 1998..Activation of MMPs by mast cell-derived proteases may be an important mechanism in atherosclerotic plaque destabilization...
The fat-fed apolipoprotein E knockout mouse brachiocephalic artery in the study of atherosclerotic plaque ruptureAndrew R Bond
Bristol Heart Institute, University of Bristol, Bristol Royal Infirmary, Bristol, UK
J Biomed Biotechnol 2011:379069. 2011..The purpose of this review is to highlight the reasons why we should be looking to the apolipoprotein E knockout mouse to further our understanding of plaque rupture...
Coronary artery disease progression is associated with increased resistance of hearts and myocytes to cardiac insultsAnabelle Chase
Faculty of Medicine and Dentistry, Bristol Heart Institute, University of Bristol, Bristol, UK
Crit Care Med 35:2344-51. 2007..To investigate whether coronary artery disease alters vulnerability of hearts and myocytes to cardiac insults. To address this issue, we developed an experimental model of coronary artery disease...
Effect of transglutaminase 2 (TG2) deficiency on atherosclerotic plaque stability in the apolipoprotein E deficient mouseHelen Williams
Bristol Heart Institute, University of Bristol, Level 7, Bristol Royal Infirmary, Bristol BS2 8HW, UK
Atherosclerosis 210:94-9. 2010..TG2 is also expressed within plaques that develop within the brachiocephalic arteries of apolipoprotein E (apoE) deficient mice...
Divergent effects of matrix metalloproteinases 3, 7, 9, and 12 on atherosclerotic plaque stability in mouse brachiocephalic arteriesJason L Johnson
Bristol Heart Institute, University of Bristol, Bristol BS2 8HW, United Kingdom
Proc Natl Acad Sci U S A 102:15575-80. 2005..These data demonstrate that MMPs are directly involved in atherosclerotic plaque destabilization and clearly show that members of the MMP family have widely differing effects on atherogenesis...
Moderately elevated plasma homocysteine impairs functional endothelial recovery following denudation of mouse carotid arteriesAlastair L Miller
Bristol Heart Institute, University of Bristol, Bristol, UK
Metabolism 53:760-5. 2004..69, P <.003). These data suggest that even modest homocysteinemia has a deleterious effect on the function of healed endothelium in mouse arteries. This may account for its adverse influence on chronic cardiovascular disease...
Delayed recovery of receptor-mediated functional responses to acetylcholine in mouse isolated carotid arteries following endothelial denudation in vivoAlastair L Miller
Bristol Heart Institute, University of Bristol, Bristol, UK
J Vasc Res 40:449-59. 2003....
Ruptures of delight? A new mouse model of plaque ruptureChristopher L Jackson
Arterioscler Thromb Vasc Biol 26:1191-2. 2006
Defining and defending murine models of plaque ruptureChristopher L Jackson
Arterioscler Thromb Vasc Biol 27:973-7. 2007
