Institute of Preventive Medicine, School of Public Health, Dali University, No. 22, Wanhua Road, Dali, Yunnan, 671000, People's Republic of China.
Sichuan Tianfu New Area Public Health Center, Zhengxing Street, Chengdu, Sichuan, 610218, People's Republic of China.
Sci Rep. 2024 Aug 16;14(1):18962. doi: 10.1038/s41598-024-69937-9.
Cadmium, a common metal pollutant, has been demonstrated to induce type 2 diabetes by disrupting pancreatic β cells function. In this study, transcriptome microarray was utilized to identify differential gene expression in oxidative damage to pancreatic β cells following cadmium exposure. The results indicated that a series of mRNAs, LncRNAs, and miRNAs were altered. Of the differentially expressed miRNAs, miR-29a-3p exhibited the most pronounced alteration, with an 11.62-fold increase relative to the control group. Following this, the target gene of miR-29a-3p was identified as Col3a1 through three databases (miRDB, miRTarbase and Tarbase), which demonstrated a decrease across the transcriptome microarray. The upstream target gene of miR-29a-3p was identified as NONMMUT036805, with decreased expression observed in the microarray. Finally, the expression trend of NONMMUT036805/miR-29a-3p/Col3a1 was reversed following NAC pretreatment. This was accompanied by a reduction in oxidative damage indicators, MDA/ROS/GSH-Px appeared to be negatively affected to varying degrees. In conclusion, this study has demonstrated that multiple RNAs are altered during cadmium exposure-induced oxidative damage in pancreatic β cells. The NONMMUT036805/miR-29a-3p/Col3a1 axis has been shown to be involved in this process, which provides a foundation for the identification of potential targets for cadmium toxicity intervention.
镉是一种常见的金属污染物,已被证明通过破坏胰腺β细胞功能诱导 2 型糖尿病。在这项研究中,利用转录组微阵列技术来识别镉暴露后胰腺β细胞氧化损伤的差异基因表达。结果表明,一系列 mRNAs、lncRNAs 和 miRNAs 发生了改变。在差异表达的 miRNAs 中,miR-29a-3p 表现出最显著的改变,与对照组相比增加了 11.62 倍。随后,通过三个数据库(miRDB、miRTarbase 和 Tarbase)鉴定出 miR-29a-3p 的靶基因 Col3a1,该基因在转录组微阵列中呈下降趋势。miR-29a-3p 的上游靶基因被鉴定为 NONMMUT036805,微阵列中观察到该基因表达下降。最后,NAC 预处理后 NONMMUT036805/miR-29a-3p/Col3a1 的表达趋势发生逆转。同时,氧化损伤标志物 MDA/ROS/GSH-Px 的表达也受到不同程度的影响。总之,本研究表明,在镉暴露诱导的胰腺β细胞氧化损伤中,多种 RNA 发生改变。NONMMUT036805/miR-29a-3p/Col3a1 轴参与了这一过程,为镉毒性干预的潜在靶点识别提供了依据。