• PATHWAY
  • Conclusions −These results suggest a novel 2-step pathway for increased tissue factor activity on smooth muscle cell surfaces in which lipoproteins regulate synthesis of a latent tissue factor and oxidants activate the protein complex. (ahajournals.org)
  • cell
  • Tissue factor expression on the smooth muscle cell surface could be of pathological significance as a contributor to plaque growth, thrombus formation, and the acute coronary syndrome after plaque rupture. (ahajournals.org)
  • Professor Julie Campbell, Cell Biologist and Professorial Fellow at the Australian Institute for Bioengineering and Nanotechnology is recognized as a world leader in the field of smooth muscle biology. (wikipedia.org)
  • Julie Hazel Campbell is a cell biologist specializing in vascular smooth muscle. (wikipedia.org)
  • 1990
  • Rembold, C. M. and Murphy, R. A., 1990, Latch-bridge model in smooth muscle: [Ca 2+ ] i can quantitatively predict stress, Am. J. Physiol . (springer.com)
  • involves
  • She has other research that involves basic cellular interactions in the artery wall, and the definition of single transduction pathways through which factors act to enhance vascular disease regression and prevent disease development/progression. (wikipedia.org)
  • Effects
  • We investigated the effects of corticosterone (10 −6 to 10 −12 mol/L) on early vascular mineralocorticoid receptor signaling by Western blotting, confocal microscopy, and myography. (ahajournals.org)
  • All effects of the catecholamines adrenaline, noradrenaline, dopamine and isoprenaline could be accounted for by an action as agonists, activating substances, on α- und β-adrenoceptors co-existing in vascular smooth muscle. (wikipedia.org)
  • Effects of visnadine on rat isolated vascular smooth muscles. (wikipedia.org)
  • pathways
  • These new mineralocorticoid receptor-dependent signaling pathways suggest that glucocorticoids may contribute to vascular disease via mineralocorticoid receptor signaling, independent of circulating aldosterone. (ahajournals.org)
  • 1986
  • Ca 2+ binding to troponin and the resulting thin filament conformational change acts as a switch in striated muscle that enables crossbridges to bind to actin and cycle (Rüegg, 1986). (springer.com)
  • decrease
  • This improvement in performance of the ventricles is likely to result from a direct stimulation of the depressed myocardium as well as a decrease in peripheral vascular resistance. (wikipedia.org)
  • disease
  • Although there is evidence for a two-hit mechanism (germline and somatic inactivation of two PKD alleles) explaining the focal development of renal and hepatic cysts, haploinsufficiency is more likely to account for the vascular manifestations of the disease. (wikipedia.org)
  • consumption
  • Vascular smooth muscle contracts or relaxes to change both the volume of blood vessels and the local blood pressure, a mechanism that is responsible for the redistribution of the blood within the body to areas where it is needed (i.e. areas with temporarily enhanced oxygen consumption). (wikipedia.org)