科研之友
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摘要
Background and aim of the study: Valvular calcification is a prominent feature of aortic valve stenosis (AS), and calcified aortic valves share several features with bone tissue. Hypoxia-inducible factor-2 (HIF-2) is activated by nuclear factor-kappa B (NE-kappa B) and plays a critical role in an osteoblastic differentiation. The study aim was to determine whether the NF-kappa B-HIF-2 pathway is involved in the pathophysiology of calcified aortic valve disease. %26lt;br%26gt;Methods: A total of 50 specimens of aortic valve leaflets obtained from patients who had undergone aortic valve replacement for AS was examined. The aortic valve leaflets from 10 patients with annuloaortic ectasia (AAE) served as controls. The stenotic valve leaflets were examined using immunohistochemistry to detect NE-kappa B, HIF-2 alpha, vascular endothelial growth factor (VEGF), vascular endothelial cells, and collagen X. The calcification area was measured and any correlation between the calcification area and NF-kappa B-HIF-2 pathway was assessed. %26lt;br%26gt;Results: NF-kappa B and HIF-2 alpha were expressed in the leaflets from patients with AS, but not in those from AAE controls. Both factors were expressed around massive calcified lesions, and HIF-2 alpha was co-localized with NF-kappa B. VEGF, neoangiogenesis and collagen X were located in the area where HIF-2 alpha was expressed, and correlated positively with HIF-2 alpha expression. The calcification area correlated positively with collagen X expression. %26lt;br%26gt;Conclusion: The NF-kappa B-HIF-2 pathway was expressed in calcified aortic valves and associated with an increased expression of VEGF and collagen X. This signaling pathway may Play important roles in the pathophysiology of AS.
- 出版日期2014-9
