Complementary transcriptomic and proteomic analyses elucidate the toxicological molecular mechanisms of deoxynivalenol-induced contractile dysfunction in enteric smooth muscle cells
文献类型： 外文期刊
作者： Qiao, Yu 1 ; Ji, Xu 2 ; Guo, Huiduo 3 ; Zheng, Weijiang 1 ; Yao, Wen 1 ;
作者机构： 1.Nanjing Agr Univ, Coll Anim Sci & Technol, .1 Weigang Rd, Nanjing 210095, Peoples R China
2.Anhui Acad Agr Sci, Inst Anim Sci & Vet Med, Anhui Prov Key Lab Livestock & Poultry Prod Safety, Hefei 230031, Peoples R China
3.Jiangsu Univ Sci & Technol, Coll Biotechnol, Zhenjiang 212018, Peoples R China
4.Nanjing Agr Univ, Key Lab Anim Physiol & Biochem, Minist Agr & Rural Affairs Peoples Republ China, Nanjing 210095, Peoples R China
关键词： Deoxynivalenol; Enteric smooth muscle contractility; ECM-Receptor interaction; Actin polymerization; Transcriptomic; Proteomic
期刊名称：FOOD AND CHEMICAL TOXICOLOGY （ 影响因子：4.3； 五年影响因子：5.1 ）
ISSN： 0278-6915
年卷期： 2024 年 186 卷
页码：
收录情况： SCI
摘要： Deoxynivalenol (DON) is one of the frequent Fusarium mycotoxins and poses a serious threat to public health worldwide. DON-induced weight loss is tightly connected with its ability to decrease feed intake by influencing gastrointestinal tract (GIT) motility. Our previous reports indicated that DON interfered with intestinal motility by injuring the contractility of enteric smooth muscle cells (SMC). Here, we further explored the potential mechanisms by employing a complementary method of transcriptomics and proteomics using the porcine enteric smooth muscle cell line (PISMC) as an experimental model. The transcriptomic and proteomic data uncover that the expression of numerous extracellular matrix (ECM) proteins and multiple integrin subunits were downregulated in PISMC under DON exposure, suppressing the ECM-integrin receptor interaction and its mediated signaling. Furthermore, DON treatment could depress actin polymerization, as reflected by the upregulated expression of Rho GTPase-activating proteins and cofilin in PISMC. Meanwhile, the expression levels of downstream contractile apparatus genes were significantly inhibited after challenge with DON. Taken together, the current results suggest that DON inhibits enteric SMC contractility by regulating the ECM-integrin-actin polymerization signaling pathway. Our findings provide novel insights into the potential mechanisms behind the DON toxicological effects in the GIT of humans and animals.
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