HUVEC (Human Umbilical Vein Endothelial Cells) were transfected with siRNA by Magnetofection using SilenceMag beads. 68% of HUVEC were efficiently transfected.
This article highlights the capacity of Magnetofection technology to efficiently silence gene expression into human primary HUVEC with siRNA using SilenceMag from OZ Biosciences.article reference: J Am Soc Nephrol. 2014 Aug 21.
The Cardiovascular Effect of the Uremic Solute Indole-3 Acetic Acid.
Dou L, Sallée M, Cerini C, Poitevin S, Gondouin B, Jourde-Chiche N, Fallague K, Brunet P, Calaf R, Dussol B, Mallet B, Dignat-George F, Burtey S.
AbstractIn CKD, uremic solutes may induce endothelial dysfunction, inflammation, and oxidative stress, leading to increased cardiovascular risk. We investigated whether the uremic solute indole-3 acetic acid
(IAA) predicts clinical outcomes in patients with CKD and has
prooxidant and proinflammatory effects. We studied 120 patients with
CKD. During the median study period of 966 days, 29 patients died and 35
experienced a major cardiovascular event. Kaplan-Meier analysis revealed that mortality and cardiovascular
events were significantly higher in the higher IAA group (IAA>3.73
µM) than in the lower IAA group (IAA<3.73 µM). Multivariate Cox
regression analysis demonstrated that serum IAA was a significant
predictor of mortality and cardiovascular
events after adjustments for age and sex; cholesterol, systolic BP, and
smoking; C-reactive protein, phosphate, body mass index, and albumin;
diastolic BP and history of cardiovascular disease; and uremic
toxins p-cresyl sulfate and indoxyl sulfate. Notably, IAA level
remained predictive of mortality when adjusted for CKD stage. IAA levels
were positively correlated with markers of inflammation and oxidative
stress: C-reactive protein and malondialdehyde, respectively. In
cultured human endothelial cells, IAA activated an inflammatory
nongenomic aryl hydrocarbon receptor (AhR)/p38MAPK/NF-κB pathway that
induced the proinflammatory enzyme cyclooxygenase-2. Additionally, IAA
increased production of endothelial reactive oxygen species. In
conclusion, serum IAA may be an independent predictor of mortality and cardiovascular
events in patients with CKD. In vitro, IAA induces endothelial
inflammation and oxidative stress and activates an inflammatory
AhR/p38MAPK/NF-κB pathway.
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