| First Author | Zhu D | Year | 2013 |
| Journal | Mol Cell Endocrinol | Volume | 372 |
| Issue | 1-2 | Pages | 1-11 |
| PubMed ID | 23523568 | Mgi Jnum | J:201223 |
| Mgi Id | MGI:5512808 | Doi | 10.1016/j.mce.2013.03.008 |
| Citation | Zhu D, et al. (2013) A protective role for FGF-23 in local defence against disrupted arterial wall integrity?. Mol Cell Endocrinol 372(1-2):1-11 |
| abstractText | 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 d period. FGF-23 mRNA expression was significantly up-regulated by 7d (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 inhibitor of FGFR1 and FGFR3, 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 muM; 41.3% increase; P<0.01). Use of FGF-23 may represent a novel therapeutic strategy for inhibiting vascular calcification. |
