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The long noncoding RNA lnc-H3f3b2 regulates cow barn PM2.5-induced apoptosis of rat alveolar II epithelial cells through a ceRNA mechanism

文献类型： 外文期刊

作者： Sun, Yize 1 ; Sun, Ke 1 ; Du, Xiaohui 1 ; Ma, Zhenhua 1 ; Zhang, Xiqing 1 ; Yu, Xiuzhen 2 ; Gao, Yunhang 1 ;

作者机构： 1.Jilin Agr Univ, Coll Anim Sci & Technol, Changchun 130118, Peoples R China

2.Xinjiang Acad Agr Sci, Inst Agr Mechanisat, Urumqi 830091, Peoples R China

关键词： Cowshed PM 2.5; Lnc-H3f3b2; RASSF2; Apoptosis

期刊名称：ECOTOXICOLOGY AND ENVIRONMENTAL SAFETY （ 影响因子：6.1； 五年影响因子：6.4 ）

ISSN： 0147-6513

年卷期： 2025 年 302 卷

页码：

收录情况： SCI

摘要： PM2.5, a complex and toxic environmental pollutant, poses a significant threat to animal lung health. Competitive endogenous ribonucleic acids (ceRNAs) serve as a crucial regulatory mechanism for tissue damage and apoptosis and are intimately associated with the toxicity mechanism of PM2.5. However, the specific mechanism of ceRNA in lung injury and apoptosis induced by PM2.5 in cow barns remains to be fully elucidated. To address this knowledge gap, an in vivo model of rats exposed to PM2.5 in cow barns and an in vitro model of cell injury were developed. The study identified differentially expressed Lnc-H3f3b2 and constructed the LncR-H3f3b2/miR122-5p/RASSF2 regulatory network using a dual luciferase reporter gene. The results of this study demonstrated that exposure to PM2.5 led to tissue damage and a reduction in cell viability. Furthermore, the study revealed that RASSF2 overexpression could inhibit apoptosis and that lncRNA could upregulate RASSF2 levels, thereby alleviating apoptosis. This study is the first to demonstrate that this regulatory axis affects cattle lung injury induced by PM2.5 and the mechanisms of apoptosis.

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