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首页> 外文会议>Society for Biomaterials Transaction of the 31st Annual Meeting vol.XXIX pt.2 >Osteoblast Response to Surface Microtopography is Modulated by Caveolin-1
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Osteoblast Response to Surface Microtopography is Modulated by Caveolin-1

机译：Caveolin-1调节成骨细胞对表面微形貌的响应。

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Engineering orthopaedic implant surfaces to increase the rate and extent of bone growth requires a better understanding of the underlying mechanisms involved in the response of osteoblasts to surface microtopography and surface chemistry. Anchorage dependent cells like osteoblasts interact with proteins on the surface via receptors called integrins. We and others have found that integrin expression is surface dependent, suggesting that changes in integrin signaling mediate osteoblast responses to their substrate. Recent studies indicate that integrins can localize and that α_2β_1 integrin clustering can activate caveolae-mediated endocytosis in a PKCα-dependent manner. The PKCα-signaling pathway is also used by the vitamin D metabolite 1α,25(OH)_2D_3, and intact caveolae are required for 1α,25(OH)_2D_3-dependent activation of PKC. Cross-talk between the two pathways may contribute to synergistic effects of rough surface microarchitecture and 1α,25(OH)_2D_3 on osteoblastic differentiation. Caveolap are cholesterol-rich specialized regions of the plasma membrane. Caveolin-1 is the major scaffolding protein present in caveolae, providing structural support for organizing multiple components of membrane-associated signaling pathways. In addition, both the traditional nuclear vitamin D receptor (VDR) and the membrane 1α,25(OH)_2D_3 receptor ERp60 have been reported to be in caveolae. These studies suggest that caveolae and caveolin-1 might provide a site for synergy between surface dependent integrin signaling and signaling initiated by the vitamin D metabolite. To test this hypothesis, we took advantage of a caveolin-1 knockout mouse model [Cav-1(-/-)] in which the cells lack caveolae. For the experiments described below, osteoblasts were isolated from the calvaria of these mice and their response to surface microarchitecture and 1α, 25(OH)_2D_3 was compared to that of wild-type mice.
机译：工程化整形外科植入物表面以增加骨生长的速度和程度，需要更好地了解成骨细胞对表面微形貌和表面化学反应所涉及的潜在机制。诸如成骨细胞的锚定依赖性细胞通过称为整联蛋白的受体与表面蛋白相互作用。我们和其他人发现整联蛋白表达是表面依赖性的，表明整联蛋白信号传导的变化介导了成骨细胞对其底物的反应。最近的研究表明，整联蛋白可以定位并且α_2β_1整联蛋白簇可以PKCα依赖性方式激活小窝介导的内吞作用。维生素D代谢物1α，25（OH）_2D_3也使用PKCα信号通路，完整的小窝是1α，25（OH）_2D_3依赖性PKC激活所必需的。两种途径之间的串扰可能有助于粗糙表面微结构和1α，25（OH）_2D_3对成骨细胞分化的协同作用。 Caveolap是质膜富含胆固醇的专门区域。 Caveolin-1是存在于小窝中的主要支架蛋白，为组织膜相关信号通路的多个成分提供结构支持。此外，传统的核维生素D受体（VDR）和膜1α，25（OH）_2D_3受体ERp60均被报道在小窝中。这些研究表明，caveolae和caveolin-1可能为表面依赖性整合素信号传导和维生素D代谢物引发的信号传导之间的协同作用提供一个场所。为了验证这一假设，我们利用了一个caveolin-1基因敲除小鼠模型[Cav-1（-/-）]，其中的细胞缺乏caveolae。对于以下所述的实验，从这些小鼠的颅骨中分离出成骨细胞，并将其对表面微结构和1α，25（OH）_2D_3的反应与野生型小鼠的相比。

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