β-Catenin regulates ovarian granulosa cell cycle and proliferation in laying hens by interacting with TCF4

Ma, Xueying; Han, Xu; Wang, Wenwen; Zhang, Qin; Tang, Hui

doi:10.1016/j.psj.2023.103377

Cited by 2 publications

(1 citation statement)

References 42 publications

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“…Therefore, we investigated the role of TCF4 in Gln-induced cell proliferation using TCF4 siRNA and inhibitors. Xueying Ma et al showed that overexpression of TCF4 significantly promoted the proliferation of granulosa cells in stratified follicles, and another study reported that overexpression of TCF4 promoted erythrocyte development; loss of TCF4 in hippocampal nestin-expressing progenitor cells also led to loss of proliferative capacity and acquisition of bone marrow inflammatory properties . These results are similar to our study, in which Gln-promoted cell proliferation was significantly inhibited by TCF4 siRNA and an inhibitor (PKF).…”

Section: Discussionsupporting

confidence: 91%

Glutamine Promotes Porcine Intestinal Epithelial Cell Proliferation through the Wnt/β-Catenin Pathway

Fang,

Lu,

Cheng

et al. 2024

J. Agric. Food Chem.

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Glutamine (Gln) is a critical nutrient required by neonatal mammals for intestinal growth, especially for newborn piglets. However, the mechanisms underlying the role of Gln in porcine intestinal epithelium development are not fully understood. The objective of the current study was to explore the possible signaling pathway involved in the promotion of porcine intestinal epithelial cell (IPEC-J2) proliferation by Gln. The results showed that 1 mM Gln promoted IPEC-J2 cell proliferation, and tandem mass tag proteomics revealed 973 differentially expressed proteins in Gln-treated IPEC-J2 cells, 824 of which were upregulated and 149 of which were downregulated. Moreover, gene set enrichment analysis indicated that the Wnt signaling pathway is activated by Gln treatment. Western blotting analysis further confirmed that Gln activated the Wnt/β-catenin signaling pathway. In addition, Gln increased not only cytosolic β-catenin but also nuclear β-catenin protein expression. LF3 (a β-catenin/TCF4 interaction inhibitor) assay and β-catenin knockdown demonstrated that Gln-mediated promotion of Wnt/β-catenin signaling and cell proliferation were blocked. Furthermore, the inhibition of TCF4 expression suppressed Gln-induced cell proliferation. These findings further confirmed that Wnt/β-catenin signaling is involved in the promotion of IPEC-J2 cell proliferation by Gln. Collectively, these findings demonstrated that Gln positively regulated IPEC-J2 cell proliferation through the Wnt/β-catenin pathway. These data greatly enhance the current understanding of the mechanism by which Gln regulates intestinal development.

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Section: Discussionsupporting

confidence: 91%