Noncollagenous bone matrix proteins as a part of calcific aortic valve disease regulation
Noncollagenous bone matrix proteins as a part of calcific aortic valve disease regulation
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DOI：
10.1016/j.humpath.2008.04.015
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发表时间：
2008-11-01
期刊：
影响因子：
3.3
通讯作者：
Satta, Jari
中科院分区：
文献类型：
--
作者：
Pohjolainen, Virva;Taskinen, Panu;Satta, Jari
临床上，钙化主动脉瓣疾病是从阻塞性纤维（硬化）瓣膜增厚到主动脉瓣狭窄的进行性连续体。最近的证据表明，除了非骨杂项矿化之外，钙化瓣膜还表现出主动骨重塑的明显迹象。在这种情况下，非胶原骨相关蛋白被认为具有关键作用。通过逆转录酶聚合酶链式反应 (n = 31) 和免疫标记 (n = 83) 在从健康柔韧瓣膜到严重钙化瓣膜的临床连续体中检查 5 种骨基质蛋白（骨形态发生蛋白 -2 和 -4、骨唾液蛋白 II、骨桥蛋白和骨保护素）的表达。作为已知的结构性病理征兆，还检查了新生血管形成的程度。我们观察到骨桥蛋白基因表达逐渐增加（7.4 倍升高，P
Clinically, calcific aortic valve disease is a progressive continuum from obstructive fibro (sclero)tic valve thickening to aortic stenosis. Recent evidence suggests that, in addition to nonbone miscellaneous mineralization, calcified valves present distinct signs of active bone remodeling; and in this context, noncollagenous bone-associated proteins are assumed to have a critical role. The expression of 5 bone matrix proteins-bone morphogenetic protein-2 and -4, bone sialoprotein II, osteopontin, and osteoprotegerin-was examined by reverse transcriptase polymerase chain reaction (n = 31) and immunolabeling (n = 83) in the clinical continuum from healthy pliable valves to heavily calcified ones. As a known structural pathologic sign, the extent of neovascularization was also examined. We observed progressive increase in the gene expression of osteopontin (7.4-fold elevation, P