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破坏Sox21介导的毛干表皮分化引起小鼠循环脱发

发布时间 2009-07-29 浏览量 作者: 无 来源: 生物无忧

博川报道:

头发再生是一个周期性的循环过程,包括定期再生干细胞依赖性的毛囊。目前还不清楚毛囊分层分化的细胞和分子机制。我们建立了一个特异性破坏Sox21基因的小鼠循环型脱发模型,该基因编码HMG-box蛋白。这些小鼠在第一个毛囊的形态发生后表现出逐步脱发,成为完全裸体后,头发又出现再生现象。

Sox21基因在小鼠和人的毛干鳞片层和前体细胞中表达。这种基因缺乏导致了锚定毛干在毛囊的联锁结构缺失。此外,Sox21缺失小鼠的毛干角质层表达的角蛋白和角白结合蛋白也特异性的被下调,它们是Sox21编码的。这些结果表明,Sox21是毛干角质层分化的主要调控子,同时也揭示人类头发失调的可能原因。

博川推荐原文检索:

The disruption of Sox21-mediated hair shaft cuticle differentiation causes cyclic alopecia in mice

Abstract

Hair is maintained through a cyclic process that includes periodic regeneration of hair follicles in a stem cell-dependent manner. Little is known, however, about the cellular and molecular mechanisms that regulate the layered differentiation of the hair follicle. We have established a mutant mouse with a cyclic alopecia phenotype resulting from the targeted disruption of Sox21, a gene that encodes a HMG-box protein. These mice exhibit progressive hair loss after morphogenesis of the first hair follicle and become completely nude in appearance, but then show hair regrowth.

Sox21 is expressed in the cuticle layer and the progenitor cells of the hair shaft in both mouse and human. The lack of this gene results in a loss of the interlocking structures required for anchoring the hair shaft in the hair follicle. Furthermore, the expression of genes encoding the keratins and keratin binding proteins in the hair shaft cuticle are also specifically down-regulated in the Sox21-null mouse. These results indicate that Sox21 is a master regulator of hair shaft cuticle differentiation and shed light on the possible causes of human hair disorders.

原文链接"A key step for the future will be to identify the cellular pathways that are affected by these cyclic peptide原:( pnas网站相关报道(英文))

http://www.pnas.org/content/early/2009/05/25/0808324106

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