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*
Unit for Metabolic Medicine, Department of Endocrinology, Diabetes and
Internal Medicine, GKT School of Medicine, King's College London, Guy's
Hospital Campus, London, United Kingdom.
Department of Nephrology and Transplantation, Division of Medicine, GKT
School of Medicine, King's College London, Guy's Hospital Campus, London,
United Kingdom.
Correspondence to GianCarlo Viberti, Unit for Metabolic Medicine, 5th Floor, Thomas Guy House, Guy's Hospital, London, SE1 9RT, United Kingdom. Phone: 0171 955 4826; Fax: 0171 955 2985; E-mail: g.viberti{at}umds.ac.uk
Abstract. The antiproteinuric effect of angiotensin-converting enzyme inhibitors underscores the importance of a hemodynamic injury and the renin-angiotensin system in the proteinuria of various glomerular diseases. Vascular endothelial growth factor (VEGF), a potent promoter of vascular permeability, is induced in mesangial cells by both mechanical stretch and TGF-ß1. This study investigates the effect of TGF-ß blockade, angiotensin II (AngII), and the interaction between AngII and stretch on human mesangial cell VEGF production. Exposure to AngII (1 µM) induced a significant increase in VEGF mRNA and protein levels (1.5 ± 0.1 and 1.7 ± 0.3, respectively, fold increase over control, P < 0.05). The AngII receptor (AT1) antagonist Losartan (10 µM) prevented AngII-induced, but not stretch-induced, VEGF protein secretion (AngII 1.7 ± 0.3, AngII + Losartan 1.0 ± 0.1, P < 0.05; stretch 2.4 ± 0.4, stretch + Losartan 2.6 ± 0.5). Stretch-induced VEGF production was also unaffected by the addition of an anti-TGF-ß neutralizing antibody (stretch 2.85 ± 0.82 versus stretch + anti-TGF-ß 2.84 ± 0.01, fold increase over control). Simultaneous exposure to both AngII and stretch for 12 h had an additive effect on VEGF production (AngII 1.6 ± 0.1, stretch 2.6 ± 0.27, AngII + stretch 3.1 ± 0.35). Conversely, preexposure to stretch magnified AngII-induced VEGF protein secretion (unstretched + AngII 1.3 ± 0.0, stretched + AngII 1.9 ± 0.1, P < 0.01) with a parallel 1.5-fold increase in AT1 receptor levels. AngII and stretch can both independently induce VEGF production; in addition, mechanical stretch upregulates the AT1 receptor, enhancing the cellular response to AngII.
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