GPR41 Regulates the Proliferation of BRECs via the PIK3-AKT-mTOR Pathway.
GPR41 Regulates the Proliferation of BRECs via the PIK3-AKT-mTOR Pathway.
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DOI：
10.3390/ijms24044203
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发表时间：
2023-02-20
影响因子：
5.6
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中科院分区：
文献类型：
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短链脂肪酸(SCFAs)在调节牛瘤胃上皮细胞(BRECs)的增殖和发育中起着关键作用。G蛋白偶联受体41(Gpr41)作为单链脂肪酸的受体参与BRECs的信号转导。然而，Gpr41对BREC增殖的影响尚未报道。本研究结果表明，与野生型BRECs(WT)相比，GPR41(GRP41KD)基因敲除可抑制BRECs的增殖(p<；0.001)。RNA测序(RNA-seq)分析表明，WT和GPR41KD BREC的基因表达谱存在差异，主要差异基因集中在磷脂酰肌醇3-激酶(PIK3)信号转导、细胞周期和氨基酸转运途径(p<；0.05)。转录组数据进一步用Western印迹和qRT-PCR进行验证。与WT细胞相比，GPR41KD BRECs下调了雷帕霉素(MTOR)信号通路核心基因PIK3-蛋白激酶B(AKT)-哺乳动物靶基因PIK3、AKT、真核翻译起始因子4E结合蛋白1(4EBP1)和mTOR的水平(p<；0.01)。此外，与WT细胞相比，GPR41KD BREC下调了Cyclin D2和Cyclin E2(P<；0.001)的水平。因此，Gpr41可能通过介导PIK3-AKT-mTOR信号通路影响BRECs的增殖。
Short-chain fatty acids (SCFAs) play a pivotal role in regulating the proliferation and development of bovine rumen epithelial cells (BRECs). G protein-coupled receptor 41 (GPR41) is involved in the signal transduction in BRECs as a receptor for SCFAs. Nevertheless, the impact of GPR41 on the proliferation of BRECs has not been reported. The results of this research showed that the knockdown of GPR41 (GRP41KD) decreased BRECs proliferation compared with the wild-type BRECs (WT) (p < 0.001). The RNA sequencing (RNA-seq) analysis showed that the gene expression profiles differed between WT and GPR41KD BRECs, with the major differential genes enriched in phosphatidylinositol 3-kinase (PIK3) signaling, cell cycle, and amino acid transport pathways (p < 0.05). The transcriptome data were further validated by Western blot and qRT-PCR. It was evident that the GPR41KD BRECs downregulated the level of the PIK3-Protein kinase B (AKT)-mammalian target of the rapamycin (mTOR) signaling pathway core genes, such as PIK3, AKT, eukaryotic translation initiation factor 4E binding protein 1 (4EBP1) and mTOR contrasted with the WT cells (p < 0.01). Furthermore, the GPR41KD BRECs downregulated the level of Cyclin D2 p < 0.001) and Cyclin E2 (p < 0.05) compared with the WT cells. Therefore, it was proposed that GPR41 may affect the proliferation of BRECs by mediating the PIK3-AKT-mTOR signaling pathway.
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影响因子：
28.2
作者：
Hanrahan AJ;Schultz N;Westfal ML;Sakr RA;Giri DD;Scarperi S;Janakiraman M;Olvera N;Stevens EV;She QB;Aghajanian C;King TA;Stanchina Ed;Spriggs DR;Heguy A;Taylor BS;Sander C;Rosen N;Levine DA;Solit DB
通讯作者：
Solit DB
影响因子：
4
作者：
PANDEY, S;WANG, E
通讯作者：
WANG, E
影响因子：
7.5
作者：
Feng, Fa-Bo;Qiu, Hai-Yan
通讯作者：
Qiu, Hai-Yan
影响因子：
3.5
作者：
Kertz, A. F.;Hill, T. M.;Drackley, J. K.
通讯作者：
Drackley, J. K.
影响因子：
--
作者：
Han, Chunchun;Wei, Shouhai;Zeng, Xianyin
通讯作者：
Zeng, Xianyin