妊娠至哺乳期长期暴露于重力改变环境影响大鼠乳腺细胞骨架蛋白的丰度

Kibrom M. Alula, J. Resau, O. Patel
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引用次数: 2

摘要

催乳素(PRL)在乳腺中的致乳、致乳和造乳作用是通过一种特定的细胞因子受体——PRL受体(PRLR)介导的。PRLR锚定在细胞骨架上,其激活和随后的信号转导依赖于完整/完整的细胞骨架组织。先前的研究表明,暴露于超重(HG)的大鼠乳腺中PRLR的下调和代谢输出的减少。因此,本研究的目的是利用定量免疫组织化学来确定妊娠期间汞暴露对大鼠乳腺前和产后细胞骨架蛋白丰度的影响。妊娠大鼠从妊娠第11 ~ 20天(G20)至产后第1天(P1)和第3天(P3)暴露于2xg [HG]或1xg[静止对照(SC)]。每个小叶抗原(肌动蛋白、微管蛋白、细胞角蛋白和静脉蛋白)的光谱表征和定量(n= 3-7小叶/显微照片;使用CRi Nuance多光谱系统计算4张显微图/载玻片)。在G20和P3时,HG大鼠肌动蛋白、微管蛋白、细胞角蛋白和波形蛋白含量升高(p<0.001)。与SC相比,HG组微管蛋白、细胞角蛋白和静脉蛋白在P1时过表达(p<0.01)。这些结果表明,不典型的细胞骨架蛋白组成有助于异常乳原信号转导和产后乳腺代谢输出减少暴露于改变的惯性环境的大鼠。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Chronic Exposure to Altered Gravity During the Pregnancy-to-Lactation Transition Affects Abundance of Cytoskeletal Proteins in the Rat Mammary Gland
Abstract The mammogenic, lactogenic, and lactopoetic effects of prolactin (PRL) in the mammary gland are mediated through a specific cytokine receptor, the PRL-receptor (PRLR). PRLR is anchored to the cytoskeleton and its activation, and subsequent signal transduction, is dependent on an integral/intact cytoskeletal organization. Previous studies revealed a down-regulation of PRLR and reduced metabolic output in the mammary gland of rats exposed to hypergravity (HG). Therefore, the objective of this study was to use quantitative immunohistochemistry to determine the effects of HG exposure during pregnancy on the pre- and postpartum abundance of the cytoskeletal proteins in the rat mammary gland. Pregnant rats were exposed to either 2xg [HG] or 1xg [Stationary control (SC)] from days 11 to 20 of gestation (G20) through postpartum days 1 (P1) and 3 (P3). Spectral characterization and quantitation of each antigen (actin, tubulin, cytokeratin, and vimentin) per lobule (n=3–7 lobules/micrograph; 4 micrographs/slide) was computed using the CRi Nuance multispectral system. At G20 and P3, increased (p<0.001) amounts of actin, tubulin, cytokeratin, and vimentin were detected in HG rats. Tubulin, cytokeratin, and vimentin were overexpressed (p<0.01) in HG group compared to SC at P1. These results suggest that atypical composition of cytoskeletal proteins contribute to the aberrant lactogenic signal transduction and associated reduced postpartum mammary metabolic output in rats exposed to altered inertial environment.
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