Jason L Johnson

Summary

Affiliation: University of Bristol
Country: UK

Publications

  1. pmc Low tissue inhibitor of metalloproteinases 3 and high matrix metalloproteinase 14 levels defines a subpopulation of highly invasive foam-cell macrophages
    Jason L Johnson
    Bristol Heart Institute, University of Bristol, England
    Arterioscler Thromb Vasc Biol 28:1647-53. 2008
  2. ncbi request reprint Suppression of atherosclerotic plaque progression and instability by tissue inhibitor of metalloproteinase-2: involvement of macrophage migration and apoptosis
    Jason L Johnson
    Bristol Heart Institute, University of Bristol, Bristol, England
    Circulation 113:2435-44. 2006
  3. pmc A selective matrix metalloproteinase-12 inhibitor retards atherosclerotic plaque development in apolipoprotein E-knockout mice
    Jason L Johnson
    Bristol Heart Institute, School of Clinical Sciences, University of Bristol, Bristol, United Kingdom
    Arterioscler Thromb Vasc Biol 31:528-35. 2011
  4. ncbi request reprint Matrix metalloproteinase (MMP)-3 activates MMP-9 mediated vascular smooth muscle cell migration and neointima formation in mice
    Jason L Johnson
    Bristol Heart Institute, University of Bristol, Bristol, United Kingdom
    Arterioscler Thromb Vasc Biol 31:e35-44. 2011
  5. ncbi request reprint Genomics of foam cells and nonfoamy macrophages from rabbits identifies arginase-I as a differential regulator of nitric oxide production
    Anita C Thomas
    Bristol Heart Institute, University of Bristol, Bristol Royal Infirmary, Bristol, BS2 8HW, United Kingdom
    Arterioscler Thromb Vasc Biol 27:571-7. 2007
  6. pmc MMP-7 mediates cleavage of N-cadherin and promotes smooth muscle cell apoptosis
    Helen 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
  7. pmc Divergent effects of matrix metalloproteinases 3, 7, 9, and 12 on atherosclerotic plaque stability in mouse brachiocephalic arteries
    Jason L Johnson
    Bristol Heart Institute, University of Bristol, Bristol BS2 8HW, United Kingdom
    Proc Natl Acad Sci U S A 102:15575-80. 2005
  8. ncbi request reprint Effect of broad-spectrum matrix metalloproteinase inhibition on atherosclerotic plaque stability
    Jason L Johnson
    Bristol Heart Institute, University of Bristol, Level 7, Bristol Royal Infirmary, Bristol BS2 8HW, United Kingdom
    Cardiovasc Res 71:586-95. 2006
  9. pmc Classical macrophage activation up-regulates several matrix metalloproteinases through mitogen activated protein kinases and nuclear factor-κB
    Wei Chun Huang
    Bristol Heart Institute, University of Bristol, Bristol, United Kingdom
    PLoS ONE 7:e42507. 2012
  10. ncbi request reprint Relationship between type IV collagen degradation, metalloproteinase activity and smooth muscle cell migration and proliferation in cultured human saphenous vein
    Concepcion M Aguilera
    Bristol Heart Institute, University of Bristol, Level 7, Bristol Royal Infirmary, BS2 8HW, Bristol, UK
    Cardiovasc Res 58:679-88. 2003

Detail Information

Publications24

  1. pmc Low tissue inhibitor of metalloproteinases 3 and high matrix metalloproteinase 14 levels defines a subpopulation of highly invasive foam-cell macrophages
    Jason L Johnson
    Bristol Heart Institute, University of Bristol, England
    Arterioscler Thromb Vasc Biol 28:1647-53. 2008
    ..An excess of metalloproteinases (MMPs) over tissue inhibitors of metalloproteinases (TIMPs) may favor atherosclerotic plaque rupture. We compared TIMP levels in nonfoamy and foam-cell macrophages (FCM) generated in vivo...
  2. ncbi request reprint Suppression of atherosclerotic plaque progression and instability by tissue inhibitor of metalloproteinase-2: involvement of macrophage migration and apoptosis
    Jason 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...
  3. pmc A selective matrix metalloproteinase-12 inhibitor retards atherosclerotic plaque development in apolipoprotein E-knockout mice
    Jason 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...
  4. ncbi request reprint Matrix metalloproteinase (MMP)-3 activates MMP-9 mediated vascular smooth muscle cell migration and neointima formation in mice
    Jason L Johnson
    Bristol Heart Institute, University of Bristol, Bristol, United Kingdom
    Arterioscler Thromb Vasc Biol 31:e35-44. 2011
    ..We therefore investigated the effect of MMP-3 knockout on neointima formation after carotid ligation in vivo and VSMC migration in vitro...
  5. ncbi request reprint Genomics of foam cells and nonfoamy macrophages from rabbits identifies arginase-I as a differential regulator of nitric oxide production
    Anita C Thomas
    Bristol Heart Institute, University of Bristol, Bristol Royal Infirmary, Bristol, BS2 8HW, United Kingdom
    Arterioscler Thromb Vasc Biol 27:571-7. 2007
    ..We sought to identify genes differentially regulated in foam cells, since these are likely to include new targets for intervention...
  6. pmc MMP-7 mediates cleavage of N-cadherin and promotes smooth muscle cell apoptosis
    Helen 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...
  7. pmc Divergent effects of matrix metalloproteinases 3, 7, 9, and 12 on atherosclerotic plaque stability in mouse brachiocephalic arteries
    Jason 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...
  8. ncbi request reprint Effect of broad-spectrum matrix metalloproteinase inhibition on atherosclerotic plaque stability
    Jason L Johnson
    Bristol Heart Institute, University of Bristol, Level 7, Bristol Royal Infirmary, Bristol BS2 8HW, United Kingdom
    Cardiovasc Res 71:586-95. 2006
    ..We have therefore investigated the effects of a broad-spectrum MMP inhibitor, RS-130830, on plaque development and stability. This compound inhibits a wide range of MMPs at concentrations below 20 nmol/L...
  9. pmc Classical macrophage activation up-regulates several matrix metalloproteinases through mitogen activated protein kinases and nuclear factor-κB
    Wei Chun Huang
    Bristol Heart Institute, University of Bristol, Bristol, United Kingdom
    PLoS ONE 7:e42507. 2012
    ..The signalling pathways defined here suggest targets for selective modulation of MMP activity...
  10. ncbi request reprint Relationship between type IV collagen degradation, metalloproteinase activity and smooth muscle cell migration and proliferation in cultured human saphenous vein
    Concepcion M Aguilera
    Bristol Heart Institute, University of Bristol, Level 7, Bristol Royal Infirmary, BS2 8HW, Bristol, UK
    Cardiovasc Res 58:679-88. 2003
    ..We conclude that MMPs mediate loss of basement membrane and this is closely related to SMC migration. SMC proliferation does not require complete basement membrane degradation, which itself does not require MMPs in proliferating SMC...
  11. doi request reprint Sustained reduction of vein graft neointima formation by ex vivo TIMP-3 gene therapy
    Sarah J George
    Bristol Heart Institute, University of Bristol, Bristol, United Kingdom
    Circulation 124:S135-42. 2011
    ..However, it is essential to determine whether this approach will provide longer-term benefits...
  12. pmc Soluble N-cadherin overexpression reduces features of atherosclerotic plaque instability
    Cressida A Lyon
    Bristol Heart Institute, Bristol Royal Infirmary, UK
    Arterioscler Thromb Vasc Biol 29:195-201. 2009
    ..We previously demonstrated that N-cadherin, a cell-cell adhesion molecule, reduces VSMC apoptosis in vitro. In this study, we examined whether a soluble form of N-cadherin (SNC) affected VSMC apoptosis and plaque stability...
  13. doi request reprint Role of colony-stimulating factors in atherosclerosis
    Karina Di Gregoli
    Laboratory of Cardiovascular Pathology, School of Clinical Sciences, University of Bristol, Bristol Royal Infirmary, Bristol, UK
    Curr Opin Lipidol 23:412-21. 2012
    ....
  14. ncbi request reprint Transforming growth factor-beta is activated by plasmin and inhibits smooth muscle cell death in human saphenous vein
    Sarah J George
    Bristol Heart Institute, University of Bristol, Bristol, UK
    J Vasc Res 42:247-54. 2005
    ..The effect of activation of endogenous transforming growth factor-beta (TGF-beta) on smooth muscle cell apoptosis was assessed in human saphenous vein...
  15. doi request reprint Wnt4/β-catenin signaling induces VSMC proliferation and is associated with intimal thickening
    Aikaterini Tsaousi
    Bristol Heart Institute, University of Bristol, Bristol Royal Infirmary, Bristol, United Kingdom
    Circ Res 108:427-36. 2011
    ..Vascular smooth muscle cell (VSMC) proliferation causes intimal thickening in atherosclerosis and restenosis. Previously, we demonstrated that Wnt/β-catenin signaling upregulates VSMC proliferation in vitro...
  16. ncbi request reprint A bioabsorbable (polyglactin), nonrestrictive, external sheath inhibits porcine saphenous vein graft thickening
    Jamie Y Jeremy
    The Bristol Heart Institute, Bristol Royal Infirmary, University of Bristol, Bristol, UK
    J Thorac Cardiovasc Surg 127:1766-72. 2004
    ..The effect of external macro-porous biodegradable (polyglactin) sheaths on neointimal and medial thickening in porcine vein grafts was therefore investigated...
  17. ncbi request reprint Assessment of unstable atherosclerosis in mice
    Christopher 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...
  18. pmc Macrophage heterogeneity in atherosclerotic plaques
    Jason L Johnson
    Bristol Heart Institute, University of Bristol, Level 7, Bristol Royal Infirmary, Bristol BS2 8HW, UK
    Curr Opin Lipidol 20:370-8. 2009
    ..The varied behaviour of macrophages and foam cells during atherosclerosis and its clinical sequelae prompt the question whether all these activities can be the property of a single cell population...
  19. doi request reprint In situ zymography
    Sarah J George
    Bristol Heart Institute, Bristol Royal Infirmary, University of Bristol, Bristol, UK
    Methods Mol Biol 622:271-7. 2010
    ..Additionally, this technique can be adapted for use with cell cultures, permitting precise location of MMP activity within cells, time-lapse analysis of MMP activity and analysis of MMP activity in migrating cells...
  20. pmc Vulnerable atherosclerotic plaque metalloproteinases and foam cell phenotypes
    Andrew C Newby
    Bristol Heart Institute, Bristol Royal Infirmary, Bristol BS2 8HW, UK
    Thromb Haemost 101:1006-11. 2009
    ..These phenotypes could play differing roles in cap, core and aneurysm formation...
  21. ncbi request reprint Animal models of spontaneous plaque rupture: the holy grail of experimental atherosclerosis research
    Michael E Rosenfeld
    Department of Pathobiology, University of Washington, Box 353410, Seattle 98195, USA
    Curr Atheroscler Rep 4:238-42. 2002
    ....
  22. ncbi request reprint Orally administered penicillamine is a potent inhibitor of neointimal and medial thickening in porcine saphenous vein-carotid artery interposition grafts
    Song Wan
    Department of Surgery, Prince of Wales Hospital, Chinese University of Hong Kong, Hong Kong, China
    J Thorac Cardiovasc Surg 133:494-500. 2007
    ..This project therefore examined the effect of the copper chelator penicillamine on saphenous vein graft thickening in a pig model...
  23. ncbi request reprint Genetic strategies to elucidate the roles of matrix metalloproteinases in atherosclerotic plaque growth and stability
    Andrew C Newby
    Circ Res 97:958-60. 2005
  24. ncbi request reprint Long-term reduction of medial and intimal thickening in porcine saphenous vein grafts with a polyglactin biodegradable external sheath
    Vikram Vijayan
    Vascular Unit, The Bristol Royal Infirmary, Bristol BS2 8HW, UK
    J Vasc Surg 40:1011-9. 2004
    ....