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亚斯巴拉金和普罗林都需要通过ATF4减少来降低Sestrin2的mRNA水平,并调节 I型原蛋白α1链的产生和静止的RIT肝星状细胞的增殖

Ran Sawa¹, Manami Ogawa¹, Hana Suzuki¹

¹Department of Nutrition and Food Science, Kobe Women's University Graduate School of Life Sciences, Kobe 654-8585, Japan.

Biomedical reports

|April 18, 2025

概括

特定的氨基酸,阿斯巴拉金 (Asn) 和 (Pro),影响肝星细胞 (HSC) 中的塞斯特林2 (SESN2) 表达. AP补充剂减少了静止HSC中的SESN2和原 (COL1A1) mRNA,影响了纤维化研究.

科学领域:

细胞生物学细胞生物学
生物化学生化学
分子生物学分子生物学

背景情况:

塞斯特林2 (SESN2) 在包括肝损伤在内的细胞应激过程中被上调,并且可以通过激活的肝星细胞 (HSC) 抑制原蛋白合成.
氨基酸在调节SESN2表达和HSC功能,特别是参与原生产的静止HSC中的精确作用尚不清楚.

研究的目的:

研究特定的氨基酸如何影响SESN2表达和静止RI-T HSCs的功能.
阐明SESN2在HSC内原蛋白生产中的调节机制.

主要方法:

使用了逆转录定量PCR,西部涂抹和细胞增殖试验.
研究了阿斯巴拉金 (Asn) 和プロ林 (Pro) (AP) 补充剂对SESN2,ATF4和COL1A1mRNA水平的影响.
研究了SESN2和ATF4淘汰对COL1A1mRNA水平的影响.

主要成果:

在5小时内,AP补充剂显著降低了静止HSC中的SESN2和ATF4mRNA水平.
AP部分降低了COL1A1mRNA,但SESN2/ATF4敲除具有更实质性的效果,表明SESN2独立的途径.
长期的AP补充剂增加了COL1A1的产生和细胞增殖,同时抑制了SESN2/ATF4,表明从应激反应转向增殖和合成.

结论:

由氨基酸缺乏引起的SESN2有助于调高COL1A1;然而,AP通过SESN2独立的途径影响COL1A1.
在静止的HSC中SESN2的功能似乎与其在激活的HSC中的作用不同,影响着原蛋白生产调节.
这些发现为SESN2在原蛋白合成中的调节机制以及肝纤维化的潜在治疗点提供了新的见解.

关键词:

一个RI-T细胞.塞斯特林 2 塞斯特林阿斯巴拉基因 (asparagine) 是一种原蛋白是一种原蛋白.肝脏的恒星细胞.普罗林是什么意思普罗林是什么意思

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