biowa, when you write << You are the master of the Abstract.>> I have to say that I have learned at the cyberfeet of the Real Master: Henry in the Ligand board. And thanks squetch for helping me develop this rare talent -g-
BTW, is this the PNAS (do not tell the boys at VD Inc. how "PNAS" is sometimes pronounced -g-) paper?
Proc Natl Acad Sci U S A 93 (19): 10417-10422 (Sep 17 1996)
Identification of vascular endothelial genes differentially responsive
to fluid mechanical stimuli: cyclooxygenase-2, manganese
superoxide dismutase, and endothelial cell nitric oxide synthase are
selectively up-regulated by steady laminar shear stress.
Topper JN, Cai J, Falb D, Gimbrone MA Jr
Department of Pathology, Brigham and Women's Hospital, Boston, MA 02115, USA.
Early atherosclerotic lesions develop in a topographical pattern that strongly suggests involvement of hemodynamic
forces in their pathogenesis. We hypothesized that certain endothelial genes, which exhibit differential responsiveness to
distinct fluid mechanical stimuli, may participate in the atherogenic process by modulating, on a local level within the
arterial wall, the effects of systemic risk factors. A differential display strategy using cultured human endothelial cells
has identified two genes, manganese superoxide dismutase and cyclooxygenase-2, that exhibit selective and sustained
up-regulation by steady laminar shear stress (LSS). Turbulent shear stress, a nonlaminar fluid mechanical stimulus,
does not induce these genes. The endothelial form of nitric oxide synthase also demonstrates a similar LSS-selective
pattern of induction. Thus, three genes with potential atheroprotective (antioxidant, antithrombotic, and antiadhesive)
activities manifest a differential response to distinct fluid mechanical stimuli, providing a possible mechanistic link
between endothelial gene expression and early events in atherogenesis. The activities of these and other LSS-responsive
genes may have important implications for the pathogenesis and prevention of atherosclerosis. |
