miR-122-5p Promotes Cowshed Particulate Matter2.5-Induced Apoptosis in NR8383 by Targeting COL4A1
文献类型： 外文期刊
作者： Sun, Yize 1 ; Sun, Ke 1 ; Ma, Zhenhua 1 ; Zhang, Xiqing 1 ; Du, Xiaohui 1 ; Jia, Yunna 1 ; Zhu, Yanbin 2 ; Inam, Muhammad 3 ; Gao, Yunhang 1 ; Basang, Wangdui 2 ;
作者机构： 1.Jilin Agr Univ, Coll Anim Sci & Technol, Dept Vet Med, Changchun 130118, Peoples R China
2.Tibet Acad Agr & Anim Husb Sci, Inst Anim Husb & Vet Med, Lhasa 850009, Peoples R China
3.Shaheed Benazir Bhutto Univ Sheringal, Dept Zool, Dir Upper 18050, Pakistan
关键词： PM2.5; microRNA; ECM; PI3K/AKT; apoptosis
期刊名称：TOXICS （ 影响因子：3.9； 五年影响因子：4.2 ）
ISSN：
年卷期： 2024 年 12 卷 6 期
页码：
收录情况： SCI
摘要： It is well known that Particulate Matter2.5 (PM2.5) has a major adverse effect on the organism. However, the health hazards of livestock farm PM2.5 to humans and animals are not yet known, and the role of miRNAs in the cellular damage induced by livestock farm PM2.5 is also unclear. Therefore, our study used cowshed PM2.5 to stimulate rat alveolar macrophage NR8383 to construct an in vitro injury model to investigate the effect of miR-122-5p on PM2.5-induced apoptosis in the NR8383. The level of apoptosis was quantified by flow cytometry and Hoechst 33342/PI double staining. Furthermore, the potential target gene Collagen type IV alpha (COL4A1) of miR-122-5p was identified through the use of bioinformatics methods. The results demonstrated a decline in cell viability and an increase in apoptosis with rising PM2.5 concentrations and exposure durations. The transfection of miR-122-5p mimics resulted in an upregulation of the pro-apoptotic protein Bcl-xL/Bcl-2 and activation of cleaved caspase-3 while inhibiting the anti-apoptotic protein B-cell lymphoma-2. The experimental data indicate that miR-122-5p is involved in the apoptotic process by targeting COL4A1. Furthermore, the overexpression of COL4A1 was observed to enhance the PM2.5-activated PI3K/AKT/NF-kappa B signaling pathway, which contributed to the inhibition of apoptosis. This finding offers a promising avenue for the development of therapeutic strategies aimed at mitigating cellular damage induced by PM2.5 exposure.
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