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成人肾上腺皮质以一种特定方式快速组织更新
作者:小柯机器人 发布时间:2019/8/6 20:12:35

法国蔚蓝海岸大学Andreas Schedl研究组的一项最新研究发现成人肾上腺皮质以一种性别特异性的方式进行组织的快速更新。 这一研究成果于2019年8月发表在国际顶尖学术期刊《细胞—干细胞》上。

进化导致了两性之间的深刻差异,该差异进一步延伸到非生殖器官,并反映在疾病的易感性和进展上。然而,这些差异的细胞和分子机理在很大程度上仍然未知。

研究团队报告肾上腺组织更新是非常活跃的,且性别差异明显,雌性小鼠的更新速度比雄性小鼠快三倍。此外,雄性的体内平衡依赖于激素生成区细胞的增殖,但雌性会使用肾上腺囊内的额外的干祖细胞。通过谱系追踪、性别逆转模型、性腺切除和双氢睾酮治疗,该研究团队进一步表明,性别特异性干细胞的活性是由抑制腺囊中Gli 1+干细胞增长和细胞增殖的雄性激素所驱动的。综上所述,他们的发现为肾上腺性别二态性提供了分子和细胞基础,或许可以解释女性肾上腺疾病发病率的增加。

附:英文原文

Title: The Adult Adrenal Cortex Undergoes Rapid Tissue Renewal in a Sex-Specific Manner

Author: Analle Grabek, Bastien Dolfi, Bryan Klein, Fariba Jian-Motamedi, Marie-Christine Chaboissier, Andreas Schedl

Issue&Volume: Volume 25 Issue 2

Abstract: Evolution has resulted in profound differences between males and females that extend to non-reproductive organs and are reflected in the susceptibility and progression of diseases. However, the cellular and molecular basis for these differences remains largely unknown. Here we report that adrenal gland tissue renewal is highly active and sexually dimorphic, with female mice showing a 3-fold higher turnover than males. Moreover, in males, homeostasis relies on proliferation of cells within the steroidogenic zone, but females employ an additional stem and/or progenitor compartment situated in the adrenal capsule. Using lineage tracing, sex reversal models, gonadectomy, and dihydrotestosterone treatments, we further show that sex-specific stem cell activity is driven by male hormones that repress recruitment of Gli1 + stem cells from the capsule and cell proliferation. Taken together, our findings provide a molecular and cellular basis for adrenal sex dimorphism that may contribute to the increased incidence of adrenal diseases in females.

DOI: https://doi.org/10.1016/j.stem.2019.04.012

Source: https://www.cell.com/cell-stem-cell/fulltext/S1934-5909(19)30161-4

期刊信息

Cell Stem Cell:《细胞—干细胞》,创刊于2007年。隶属于细胞出版社,最新IF:21.464
官方网址:https://www.cell.com/cell-stem-cell/home
投稿链接:https://www.editorialmanager.com/cell-stem-cell/default.aspx