Reach further, in an Open Access Journal Endocrinology, Diabetes & Metabolism Case Reports

ISSN 1470-3947 (print)
ISSN 1479-6848 (online)

Searchable abstracts of presentations at key conferences in endocrinology

Published by BioScientifica
Endocrine Abstracts (2010) 22 P516 

The role of fibroblast grow factor 23 in vascular calcification

Bohumil Majtan1,2, Tatsuo Shimosawa2, Rika Saito2, Hong Wang2, Shengyu Mu2, Fumiko Mori2, Yuzaburo Uetake2, Robert Holaj1 & Toshiro Fujita2

Author affiliations

Background: Patients in end stage chronic kidney disease suffer from vascular calcification have high plasma level of phosphate (PO42) and fibroblast grow factor 23 (FGF23). FGF23 is a newly identified hormone that inhibits PO42 reabsorption and downregulates expression of vitamin D in kidney.

The aim of our work was to investigate the role of FGF23 in vascular calcification.

Methods: Aortic tissue and primary culture of vascular smooth muscle cells (VSMC) both obtained from Sprague–Dawley rat were used during the experiment. Klotho plasmid was first transfected into VSMC and cultures were subsequently cultivated in high (2.6 mmol) and low (1.4 mmol) phosphate buffer solutions. Same medium was used for cultivation of aortic tissue. FGF23 was then added to cultivation medium and expression of core osteoblast-like phenotype change markers Pit-1 and Cbfa1 and involved transcription factors were examined.

Results: The expression of Pit-1 and Cbfa1 was upregulated by high PO42 and reversed after FGF23 application. This mechanism is MAPK dependent, both in vivo (aortic tissue) and in vitro (Klotho transfected VSMC). Detailed results will be presented.

Conclusion: We successfully downregulated the key osteoblast-like phenotype change markers Pit-1 and Cbfa1, which are induced by high phosphate buffer, by FGF23. This might demonstrate the possible protective effect of FGF23 in vascular calcification.

This Issue/Conference

Article tools

My recently viewed abstracts

My recent searches