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首页> 外文期刊>Journal of Cellular Physiology >Epidermal expression of the full-length extracellular calcium-sensing receptor is required for normal keratinocyte differentiation.
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Epidermal expression of the full-length extracellular calcium-sensing receptor is required for normal keratinocyte differentiation.

机译：表皮的表达完整细胞外calcium-sensing受体是正常的角化细胞分化所必需的。

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摘要

The importance of the extracellular calcium-sensing receptor (CaR) in the stringent control of extracellular Ca(2+) concentration is well established. However, the presence of CaR in tissues not directly involved in regulating mineral ion homeostasis such as the epidermis suggests a role for CaR in other cellular functions. Although extracellular Ca(2+) regulates the differentiation of epidermal keratinocytes, the role of CaR in this process in the epidermis is not fully understood. In this study we showed using in situ hybridization and immunohistochemistry that CaR is expressed in suprabasal keratinocytes of the mammalian epidermis. We then evaluated the changes in epidermal keratinocyte morphology and differentiation in Casr(-/-) mice lacking the full-length CaR. These mice show increased expression of an alternatively spliced form of CaR which lacks acute Ca(2+)-signaling properties. The absence of the full-length CaR in the epidermis resulted in ultrastructural changes (abnormal keratohyalin granule formation and precocious lamellar body secretion) in the terminally differentiated granular keratinocytes. Furthermore, the expression of both mRNA and protein for the calcium inducible keratinocyte differentiation markers, filaggrin and loricrin, were down-regulated in the epidermis of Casr(-/-) mice, whereas the number of proliferating cells were increased even though the calcium gradient within the epidermis was enhanced. Our results demonstrate that the epidermal expression of the full-length CaR is required for the normal terminal differentiation of keratinocytes.
机译：细胞外的重要性calcium-sensing受体(汽车)严格控制细胞外钙(2 +)浓度建立了。组织不直接参与调节表皮等矿物离子体内平衡显示汽车在其他细胞的作用功能。调节表皮的分化角化细胞,汽车在这个过程中的作用表皮并不完全理解。我们的研究显示使用原位杂交和免疫组织化学表达的那辆车suprabasal哺乳动物的角化细胞表皮。表皮角化细胞形态和Casr分化(- / -)小鼠缺乏完整的汽车。或者拼接的形式的表达式汽车缺乏急性Ca(2 +)信号属性。表皮导致超微结构的变化(透明角质颗粒形成和异常早熟的片状体分泌)终末分化细粒度的角质细胞。此外,两个mRNA的表达蛋白质钙诱导角化细胞丝相关蛋白和loricrin分化标记,被抑制的表皮Casr (- / -)老鼠,而增殖细胞的数量尽管钙梯度增加吗内表皮被增强。表明表皮的表达完整的汽车需要正常终端角质细胞的分化。

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