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Journal article
The antisense lncRNA of TAB2 that prevents oxidative stress to enhance the follicular growth in mammals
Communications biology, Vol.7, 1246
2024
Abstract
LncRNAs are highly implicated in oxidative stress (OS) during the growth of mammalian follicles. TAK1 binding protein 2 gene (TAB2) has been suggested to involve in the normal apoptosis and proliferation of granulosa cells (GCs), the main supporting cells in ovarian follicles. In this study, we found that TAB2 increased the expressions of SOD1, P50, and P65 to suppress the OS, thereby inhibiting the apoptosis and promoting the proliferation in GCs. Notably, DNMTs appeared to mediate the expression of TAB2 without the changes of DNA methylation at TAB2’s promoter. We identified an antisense lncRNA of TAB2, discovered that DNA methylation regulated the transcription of TAB2-AS in GCs, and found TAB2-AS medicated the follicular growth of ovaries in vivo. Mechanistically, the hypomethylation of the CpG site (−1759/−1760) activated the transcription of TAB2-AS, and the 1–155 nt and 156-241 nt of TAB2-AS were respectively complementary to 4368–4534 nt and 4215–4300 nt of TAB2’s mRNA to increase the expression of TAB2. Moreover, TAB2-AS inhibited the OS and apoptosis of GCs, while promoted the proliferation of GCs to expedite the follicular growth, which was in line with that of TAB2. Collectively, these findings revealed the antisense lncRNA mechanism mediated by DNA methylation, and TAB2-AS might be the target to control OS during follicular growth in mammals.
Details
- Title
- The antisense lncRNA of TAB2 that prevents oxidative stress to enhance the follicular growth in mammals
- Authors/Creators
- Nian Li - South China Agricultural UniversityBing YunLiqing ZengYuanyuan LvYinqi ZhouMing FangShuo Li - South China Agricultural UniversityEnyuan HuangLiuhong ZhangYao Jiang - Murdoch UniversityHao ZhangXiaolong Yuan - South China Agricultural University
- Publication Details
- Communications biology, Vol.7, 1246
- Publisher
- Springer Nature
- Identifiers
- 991005707269107891
- Copyright
- © The Author(s) 2024
- Murdoch Affiliation
- School of Medical, Molecular and Forensic Sciences
- Resource Type
- Journal article
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