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α-Glycerol monolaurate promotes tight junction proteins expression through PKC/MAPK/ATF-2 signaling pathway

文献类型： 外文期刊

作者： Dai, Siyu 1 ; Li, Cunjie 1 ; Li, Dagang 2 ; Wang, Hong 1 ;

作者机构： 1.Jinan Univ, Coll Life Sci & Technol, Guangdong Prov Engn Res Ctr Antibody Drug & Immuno, Guangzhou, Guangdong, Peoples R China

2.Guangdong Acad Agr Sci, Inst Anim Sci, Guangzhou, Guangdong, Peoples R China

关键词： intestinal epithelial cells; proteomic analysis; alpha-glycerol monolaurate; tight junction proteins; PKC/MAPK/ATF-2 signaling pathway

期刊名称：FRONTIERS IN NUTRITION （ 影响因子：5.1； 五年影响因子：5.4 ）

ISSN： 2296-861X

年卷期： 2025 年 12 卷

页码：

收录情况： SCI

摘要： Introduction: This study investigates the effects of alpha-GML on intestinal epithelial tight junction (TJ) protein expression and its molecular mechanisms. Recognizing the critical role of TJ proteins in intestinal barrier function and the potential of alpha-GML to enhance this barrier, we employ the IPEC-J2 cell model. Our aim is to validate the regulatory impact of alpha-GML on TJ protein expression and elucidate the underlying signaling pathways, thereby offering new strategies for intestinal health maintenance. Methods: Utilized Data-Independent Acquisition (DIA) analysis to identify optimal targets of alpha-GML in modulating Tight Junction (TJ) protein expression. Treated cells with specific inhibitors of PKC and MAPK to assess their role in TJ regulation by alpha-GML. Co-treated cells with the MAPK inhibitor SCH772984 and alpha-GML to study the effects on p-ATF-2 expression. Evaluated the effects of SCH772984 and ATF-2 overexpression on the protein expression levels of phosphorylated ATF-2, ZO-1, and OCLN. Results: Revealed that alpha-GML's modulation of TJ proteins might involve the PKC/MAPK signaling pathway, leading to ATF-2 phosphorylation. Both PKC and MAPK inhibitors reduced TJ protein expression (p < 0.05, p < 0.01 or p < 0.001), indicating their involvement in alpha-GML's regulation. SCH772984 counteracted alpha-GML-induced upregulation of p-ATF-2 (p < 0.05), suggesting MAPK's role in this process. Identified potential ATF-2 binding sites on ZO-1 and OCLN promoters. ATF-2 significantly enhanced ZO-1 promoter activity (p < 0.001). SCH772984 reduced phosphorylated ATF-2, ZO-1, and OCLN levels (p < 0.05 or p < 0.01), while ATF-2 overexpression rescued this decrease (p < 0.05 or p < 0.01), confirming ATF-2's role in TJ protein upregulation via the MAPK pathway. Discussion: Our study indicated that alpha-GML enhanced the expression of TJ proteins through the PKC/MAPK/ATF-2 pathway, thereby enhancing the barrier function of intestinal epithelial cells.

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