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蛋氨酸通过产生 S-腺苷甲硫氨酸来保护乳腺细胞免受氧化应激，从而维持 mTORC1 信号活性。

Methionine Protects Mammary Cells against Oxidative Stress through Producing S-Adenosylmethionine to Maintain mTORC1 Signaling Activity.

机构信息

Key Laboratory for Animal Disease Resistance Nutrition of the Ministry of Education, Animal Nutrition Institute, Sichuan Agricultural University, Chengdu 611130, China.

Adisseo France SAS, F-03600 Commentry, France.

出版信息

Oxid Med Cell Longev. 2021 Jul 19;2021:5550196. doi: 10.1155/2021/5550196. eCollection 2021.

DOI:10.1155/2021/5550196
PMID:34336098
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8315855/
Abstract

The mechanistic target of rapamycin complex 1 (mTORC1) signaling plays pivotal roles in cell growth and diseases. However, it remains mechanistically unclear about how to maintain mTORC1 activity during mammary glands development. Here we showed that mammary glands suffered from aggravated oxidative stress as pregnancy advanced and was accompanied by an increase in HO levels, while the consumption for methionine and -adenosylmethionine (SAM) rather than -adenosylhomocysteine (SAH) were promoted . Likewise, HO promoted SAM synthesis and reduced SAM utilization for methylation depending on HO levels and treatment time . HO inhibited phosphorylation of S6 kinase Thr 389 (p-S6K1 (T389)), 4E-BP1 Thr 37/46 and ULK1 Ser 757, the downstream of mTORC1, in mammary epithelial cells. However, methionine and SAM were shown to activate mTORC1 under HO-exposed condition. Moreover, this effect was not disabled by SGI-1027 which inhibits SAM transmethylation. In conclusion, methionine appeared to protect mammary cells against oxidative stress through producing SAM to maintain mTORC1 signaling activity.

摘要

雷帕霉素复合物 1（mTORC1）信号通路的作用机制在细胞生长和疾病中起着关键作用。然而，目前尚不清楚如何在乳腺发育过程中维持 mTORC1 的活性。在这里，我们发现随着妊娠的进展，乳腺受到严重的氧化应激，HO 水平升高，而蛋氨酸和 - 腺苷甲硫氨酸（SAM）的消耗而不是 - 腺苷同型半胱氨酸（SAH）被促进。同样，HO 促进 SAM 合成并减少 SAM 用于甲基化，这取决于 HO 水平和处理时间。HO 抑制乳腺上皮细胞中 mTORC1 的下游 S6 激酶 Thr 389（p-S6K1（T389））、4E-BP1 Thr 37/46 和 ULK1 Ser 757 的磷酸化。然而，在 HO 暴露的情况下，蛋氨酸和 SAM 被证明可以激活 mTORC1。此外，这种作用不会被抑制 SAM 转甲基的 SGI-1027 所阻断。总之，蛋氨酸通过产生 SAM 来保护乳腺细胞免受氧化应激，从而维持 mTORC1 信号通路的活性。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9a97/8315855/cf51741ead45/OMCL2021-5550196.007.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9a97/8315855/eb57f7953cff/OMCL2021-5550196.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9a97/8315855/561ffcf989ab/OMCL2021-5550196.002.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9a97/8315855/cf51741ead45/OMCL2021-5550196.007.jpg

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