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A Murine Pancreatic Islet Cell-based Screening for Diabetogenic Environmental Chemicals
Published on: June 25, 2018
Screening of differentially expressed RNAs and identifying a ceRNA axis during cadmium-induced oxidative damage in
Yahao Mou1,2, Yifei Sun1, Guofen Liu1
1Institute of Preventive Medicine, School of Public Health, Dali University, No. 22, Wanhua Road, Dali, Yunnan, 671000, People's Republic of China.
Abstract:
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.
Insights
Cadmium exposure damages pancreatic beta cells, altering RNA expression and increasing miR-29a-3p. The NONMMUT036805/miR-29a-3p/Col3a1 pathway is implicated in this oxidative damage.
Area of Science:
- Environmental Toxicology
- Molecular Biology
- Endocrinology
Background:
- Cadmium (Cd) is a prevalent environmental pollutant.
- Cd exposure disrupts pancreatic beta-cell function, contributing to type 2 diabetes.
- Oxidative stress is a key mechanism in Cd-induced beta-cell damage.
Purpose of the Study:
- To investigate the molecular mechanisms of Cd-induced oxidative damage in pancreatic beta cells.
- To identify key RNA molecules and pathways involved in Cd toxicity.
- To explore potential therapeutic targets for Cd-induced diabetes.
Main Methods:
- Transcriptome microarray analysis to detect differential gene expression in beta cells after Cd exposure.
- Bioinformatic analysis using miRDB, miRTarbase, and Tarbase to identify miRNA targets.
- Validation of RNA expression and oxidative stress markers (MDA, ROS, GSH-Px) with and without N-acetylcysteine (NAC) pretreatment.
Main Results:
- Cd exposure significantly altered mRNA, LncRNA, and miRNA expression in pancreatic beta cells.
- miR-29a-3p showed the most significant increase (11.62-fold).
- The NONMMUT036805/miR-29a-3p/Col3a1 axis was identified, with reversed expression trends and reduced oxidative damage markers upon NAC treatment.
Conclusions:
- Cadmium exposure induces significant alterations in RNA expression, leading to oxidative damage in pancreatic beta cells.
- The NONMMUT036805/miR-29a-3p/Col3a1 regulatory axis plays a crucial role in Cd toxicity.
- This pathway represents a potential therapeutic target for mitigating cadmium-induced diabetes.
