ECTS2013 Oral Communications Mineralisation and energy metabolism (6 abstracts)
A protective role for FGF23 in local defence against disrupted arterial wall integrity?
Dongxing Zhu 1 , Neil Mackenzie 1 , Jose Luis Millan 2 , Colin Farquharson 1 & Vicky MacRae 1
1The Roslin Institute and Royal (Dick) School of Veterinary Studies, The University of Edinburgh, Easter Bush, Roslin, Midlothian EH25 9RG, Scotland, UK; 2Sanford Children’s Health Research Center, Sanford-Burnham Medical Research Institute, La Jolla, California 92037, USA.
Increasing interest is focusing on the role of the FGF-23/Klotho axis in mediating vascular calcification. However, the underpinning mechanisms have yet to be fully elucidated. Murine VSMCs were cultured in calcifying medium for a 21-day period. FGF-23 mRNA expression was significantly up-regulated by 7 days (1.63-fold; P<0.001), with a concomitant increase in protein expression. mRNA and protein expression of both FGFR1 and Klotho were confirmed. Increased FGF-23 and Klotho protein expression was also observed in the calcified media of Enpp1−/− mouse aortic tissue. Reduced calcium deposition was observed in calcifying VSMCs cultured with recombinant FGF-23 (10 ng/ml; 28.1% decrease; P<0.01). Calcifying VSMCs treated with PD173074, an FGFR1 inhibitor, showed significantly increased calcification (50 nM; 87.8% increase; P<0.001). FGF-23 exposure induced phosphorylation of ERK1/2. Treatment with FGF-23 in combination with PD98059, an ERK1/2 inhibitor, significantly increased VSMC calcification (10 μM; 41.3% increase; P<0.01). FGF-23 may represent a novel therapeutic strategy for inhibiting vascular calcification.
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