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Shear-Induced Nitric Oxide Production by Endothelial Cells | | Krishna Sriram
; Justin G. Laughlin
; Padmini Rangamani
; Daniel M. Tartakovsky
; | | Date: |
19 May 2016 | | Abstract: | We present a biochemical model of the wall shear stress (WSS)-induced
activation of endothelial nitric oxide synthase (eNOS) in an endothelial cell
(EC). The model includes three key mechanotransducers: mechanosensing ion
channels, integrins and G-protein-coupled receptors. The reaction cascade
consists of two interconnected parts. The first is rapid activation of calcium,
which results in formation of calcium-calmodulin complexes, followed by
recruitment of eNOS from caveolae. The second is phosphoryaltion of eNOS by
protein kinases PKC and AKT. The model also includes a negative feedback loop
due to inhibition of calcium influx into the cell by cyclic guanosine
monophosphate (cGMP). In this feedback, increased nitric oxide (NO) levels
cause an increase in cGMP levels, so that cGMP inhibition of calcium influx can
limit NO production. The model was used to predict the dynamics of NO
production by an EC subjected to a step increase of WSS from zero to a finite
physiologically relevant value. Among several experimentally observed features,
the model predicts a highly nonlinear, biphasic transient behavior of eNOS
activation and NO production: a rapid initial activation due to the very rapid
influx of calcium into the cytosol (occurring within 1 to 5 minutes) is
followed by a sustained period of activation due to protein kinases. | | Source: | arXiv, 1605.5804 | | Services: | Forum | Review | PDF | Favorites | |
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