精氨酸酶 1 不会影响小鼠胎肺中 RNA m6A 的甲基化。

IF 1.6 4区 医学 Q4 DEVELOPMENTAL BIOLOGY Birth Defects Research Pub Date : 2024-02-16 DOI:10.1002/bdr2.2318
Xuesong Sui, Yanyu Sui, Peihua Long, Yifei Wang, Yu Chen, Wenjia Zhai, Lu Gao
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引用次数: 0

摘要

背景:精氨酸酶 1(Arg1)编码一种催化精氨酸代谢为鸟氨酸和尿素的关键酶。在我们最近的研究中,我们发现敲除胎儿小鼠肺中的 Arg1 会诱导上皮细胞凋亡,并显著推迟分娩的开始。N6 -甲基腺苷(m6 A)作为最丰富的内部 mRNA 修饰,已被发现在肺发育和细胞分化中发挥重要作用。然而,敲除 Arg1 是否会影响胎儿肺部的 RNA m6A 修饰仍是未知数:方法:本研究采用免疫印迹、免疫荧光和 RT-qPCR 等方法,验证了通过携带 Arg1-shRNA 的腺相关病毒敲除 Arg1 的 13.0 dpc 胎肺中 RNA m6A 水平和 RNA m6A 相关酶的表达:结果:AAV-shArg1注射小鼠与AAV-2/9注射小鼠胎肺中甲基转移酶、去甲基化酶和结合蛋白的表达无统计学差异。此外,与注射AAV-2/9的小鼠相比,注射AAV-shArg1的小鼠胎肺中总体RNA m6A水平没有明显变化:这些结果表明,精氨酸酶1并不影响小鼠胎肺中RNA m6A的甲基化,除RNA m6A修饰外,敲除Arg1对胎肺发育的影响及其与分娩启动的相互作用机制还有待进一步探讨。
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Arginase 1 does not affect RNA m6A methylation in mouse fetal lung

Background

Arginase 1 (Arg1) encodes a key enzyme that catalyzes the metabolism of arginine to ornithine and urea. In our recent study, we found that knockdown of Arg1 in the lungs of fetal mice induces apoptosis of epithelial cells and dramatically delays initiation of labor. As the most abundant internal mRNA modification, N6-methyladenosine (m6A) has been found to play important roles in lung development and cellular differentiation. However, if the knockdown of Arg1 affects the RNA m6A modification in fetal lungs remains unknown.

Methods

In the current study, the RNA m6A levels and the expression of RNA m6A related enzymes were validated in 13.0 dpc fetal lungs that Arg1 was knocked down by adeno-associated virus carrying Arg1-shRNA, using western blot, immunofluorescence, and RT-qPCR.

Results

No statistical differences were found in the expression of methyltransferase, demethylases, and binding proteins in the fetal lungs between AAV-shArg1-injected mice and AAV-2/9-injected mice. Besides, there is no significant change of overall RNA m6A level in fetal lungs from AAV-shArg1-injected mice, compared with that from AAV-2/9-injected mice.

Conclusions

These results indicate that arginase 1 does not affect RNA m6A methylation in mouse fetal lung, and the mechanisms other than RNA m6A modification underlying the effects of Arg1 knockdown on the fetal lung development and their interaction with labor initiation need to be further explored.

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来源期刊
Birth Defects Research
Birth Defects Research Medicine-Embryology
CiteScore
3.60
自引率
9.50%
发文量
153
期刊介绍: The journal Birth Defects Research publishes original research and reviews in areas related to the etiology of adverse developmental and reproductive outcome. In particular the journal is devoted to the publication of original scientific research that contributes to the understanding of the biology of embryonic development and the prenatal causative factors and mechanisms leading to adverse pregnancy outcomes, namely structural and functional birth defects, pregnancy loss, postnatal functional defects in the human population, and to the identification of prenatal factors and biological mechanisms that reduce these risks. Adverse reproductive and developmental outcomes may have genetic, environmental, nutritional or epigenetic causes. Accordingly, the journal Birth Defects Research takes an integrated, multidisciplinary approach in its organization and publication strategy. The journal Birth Defects Research contains separate sections for clinical and molecular teratology, developmental and reproductive toxicology, and reviews in developmental biology to acknowledge and accommodate the integrative nature of research in this field. Each section has a dedicated editor who is a leader in his/her field and who has full editorial authority in his/her area.
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