Renal tubular fluid shear stress promotes endothelial cell activation.

Abstract : Modified urinary fluid shear stress (FSS) induced by variations of urinary fluid flow and composition is observed in early phases of most kidney diseases. In this study, we hypothesized that changes in urinary FSS represent a tubular aggression that contributes to the development of inflammation, a key event in progression of nephropathies. Human renal tubular cells (HK-2) were exposed to FSS for 30 min at 0.01 Pa. Treatment of human endothelial cells (HMEC-1) with the resulting conditioned medium (FSS-CM) increased C-C chemokine ligand 2 (CCL2) and tumor necrosis factor (TNF)-α protein secretion, increased endothelial vascular adhesion molecule-1 (VCAM-1) mRNA expression and stimulated adhesion of human (THP-1) monocytes to the endothelial monolayer. These effects were TNF-α dependent as they were abolished by neutralization of TNF-α. Interestingly, the origin of TNF-α was not epithelial, but resulted from autocrine endothelial production. However, in contrast to short term FSS, long term FSS (5h) induced the release of the key inflammatory proteins CCL2 and TNF-α directly from tubular cells. In conclusion, these results suggest for the first time that urinary FSS can contribute to the inflammatory state involved in initiation/perpetuation of renal diseases.
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Biochemical and Biophysical Research Communications, Elsevier, 2011, 407 (4), pp.813-7. 〈10.1016/j.bbrc.2011.03.105〉
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Soumis le : vendredi 19 août 2011 - 17:11:29
Dernière modification le : mercredi 28 février 2018 - 10:23:00

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Mathieu Miravète, Julie Klein, Aurèle Besse-Patin, Julien Gonzalez, Christiane Pecher, et al.. Renal tubular fluid shear stress promotes endothelial cell activation.. Biochemical and Biophysical Research Communications, Elsevier, 2011, 407 (4), pp.813-7. 〈10.1016/j.bbrc.2011.03.105〉. 〈inserm-00615619〉

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