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首页> 外文期刊>Journal of Cellular Physiology >TGF-beta promotes cell death and suppresses lactation during the second stage of mammary involution.
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TGF-beta promotes cell death and suppresses lactation during the second stage of mammary involution.

机译：鉴定及促进细胞死亡和抑制哺乳期间乳房的第二阶段退化。

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Transforming growth factor beta (TGF-beta) ligands are known to regulate virgin mammary development and contribute to initiation of post-lactation involution. However, the role for TGF-beta during the second phase of mammary involution has not been addressed. Previously, we have used an MMTV-Cre transgene to delete exon 2 from the Tgfbr2 gene in mammary epithelium, however we observed a gradual loss of T beta RII deficient epithelial cells that precluded an accurate study of the role for TGF-beta signaling during involution timepoints. Therefore, in order to determine the role for TGF-beta during the second phase of mammary involution we have now targeted T beta RII ablation within mammary epithelium using the WAP-Cre transgene [T beta RII(WKO)Rosa26R]. Our results demonstrated that TGF-beta regulates commitment to cell death during the second phase of mammary involution. Importantly, at day 3 of mammary involution the Na-Pi type IIb co-transporter (Npt2b), a selective marker for active lactation in luminal lobular alveolar epithelium, was completely silenced in the WAP-Cre control and T beta RII(WKO)Rosa26R tissues. However, by day 7 of involution the T beta RII(WKO)Rosa26R tissues had distended lobular alveoli and regained a robust Npt2b signal that was detected at the apical luminal surface. The Npt2b abundance and localization positively correlated with elevated WAP mRNA expression, suggesting that the distended alveoli were the result of an active lactation program rather than residual milk protein and lipid accumulation. In summary, the results suggest that an epithelial cell response to TGF-beta signaling regulates commitment to cell death and suppression of lactation during the second phase of mammary involution.
机译：转化生长因子β(及)配体已知能够调节处女乳房发育并为发起post-lactation作出贡献退化。第二阶段的乳房退化被解决。MMTV-Cre转基因删除外显子2的Tgfbr2基因在乳腺上皮细胞,然而我们观察T的逐渐丧失βRII不足上皮细胞无法准确的研究的作用及信号期间退化时间点。确定的作用及在第二次我们现在的乳房退化阶段的目标TβRII消融在乳腺上皮细胞使用WAP-Cre转基因[TβRII WKO Rosa26R]。及调节细胞死亡的承诺在第二阶段的乳房退化。重要的是,在第三天的乳房退化Na-Pi IIb co-transporter Npt2b)、a型选择性标记为活跃在腔的哺乳支气管肺泡上皮,完全沉默在WAP-Cre控制和TβRII (WKO) Rosa26R组织。对合TβRII (WKO) Rosa26R组织膨胀支气管肺泡和恢复一个健壮的在顶端Npt2b信号检测腔的表面。本地化与升高呈正相关WAP mRNA表达,这表明膨胀肺泡是一个积极的结果哺乳计划而不是剩余的牛奶蛋白质和脂质积累。结果表明,一种上皮细胞反应及信号调节的承诺细胞死亡和哺乳期间的抑制第二阶段的乳房退化。

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