子宫内膜间质细胞去个体化过程中分泌通路结构和功能的深刻调整。

IF 3.6 3区 生物学 Q3 CELL BIOLOGY
Traffic Pub Date : 2022-01-01 Epub Date: 2021-10-28 DOI:10.1111/tra.12822
Tiziana Anelli, Marco Dalla Torre, Elena Borini, Elisabetta Mangini, Adele Ulisse, Claudia Semino, Roberto Sitia, Paola Panina-Bordignon
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引用次数: 2

摘要

某些类型的细胞必须扩展其胞外通路以保证蛋白质分泌的效率和保真度。一个引人注目的例子是人子宫内膜间质细胞(EnSCs)的脱个体化。在月经周期的黄体中期,黄体酮刺激诱导增殖的EnSCs分化为专业的分泌物,释放有效胚泡着床所必需的蛋白质。在这里,我们描述了人enc系(tert永生化人子宫内膜基质细胞(T-HESC))分泌途径的结构重排。与原代细胞一样,去个性化需要增殖抑制和整个分泌途径的协调扩张,而没有可检测到的未折叠蛋白反应(UPR)途径的激活。尽管一些不依赖维生素C的蛋白质的分泌受损,但在缺乏抗坏血酸的情况下,脱个体化也会发生。抗坏血酸是胶原蛋白生物生成的必要辅助因子。然而,即使在这些条件下,也无法检测到明显的UPR诱导。形态计量学分析显示,胞外通路不增加相对于细胞的体积。因此,与其他类型的细胞不同,在增殖停止后,细胞大小的协调增加保证了大量的生产。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Profound architectural and functional readjustments of the secretory pathway in decidualization of endometrial stromal cells.

Certain cell types must expand their exocytic pathway to guarantee efficiency and fidelity of protein secretion. A spectacular case is offered by decidualizing human endometrial stromal cells (EnSCs). In the midluteal phase of the menstrual cycle, progesterone stimulation induces proliferating EnSCs to differentiate into professional secretors releasing proteins essential for efficient blastocyst implantation. Here, we describe the architectural rearrangements of the secretory pathway of a human EnSC line (TERT-immortalized human endometrial stromal cells (T-HESC)). As in primary cells, decidualization entails proliferation arrest and the coordinated expansion of the entire secretory pathway without detectable activation of unfolded protein response (UPR) pathways. Decidualization proceeds also in the absence of ascorbic acid, an essential cofactor for collagen biogenesis, despite also the secretion of some proteins whose folding does not depend on vitamin C is impaired. However, even in these conditions, no overt UPR induction can be detected. Morphometric analyses reveal that the exocytic pathway does not increase relatively to the volume of the cell. Thus, differently from other cell types, abundant production is guaranteed by a coordinated increase of the cell size following arrest of proliferation.

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来源期刊
Traffic
Traffic 生物-细胞生物学
CiteScore
8.10
自引率
2.20%
发文量
50
审稿时长
2 months
期刊介绍: Traffic encourages and facilitates the publication of papers in any field relating to intracellular transport in health and disease. Traffic papers span disciplines such as developmental biology, neuroscience, innate and adaptive immunity, epithelial cell biology, intracellular pathogens and host-pathogen interactions, among others using any eukaryotic model system. Areas of particular interest include protein, nucleic acid and lipid traffic, molecular motors, intracellular pathogens, intracellular proteolysis, nuclear import and export, cytokinesis and the cell cycle, the interface between signaling and trafficking or localization, protein translocation, the cell biology of adaptive an innate immunity, organelle biogenesis, metabolism, cell polarity and organization, and organelle movement. All aspects of the structural, molecular biology, biochemistry, genetics, morphology, intracellular signaling and relationship to hereditary or infectious diseases will be covered. Manuscripts must provide a clear conceptual or mechanistic advance. The editors will reject papers that require major changes, including addition of significant experimental data or other significant revision. Traffic will consider manuscripts of any length, but encourages authors to limit their papers to 16 typeset pages or less.
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