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Updated: Jun 10, 2026
Analyses of Proteinuria, Renal Infiltration of Leukocytes, and Renal Deposition of Proteins in Lupus-prone MRL/lpr Mice
Published on: June 8, 2022
Endoplasmic reticulum stress in murine liver and kidney exposed to microcystin-LR
Wendi Qin1, Lizhi Xu, Xuxiang Zhang
1State Key Laboratory of Pollution Control and Resource Reuse, School of the Environment, Nanjing University, 22 Hankou Road, Nanjing 210093, China.
Abstract:
To investigate the effect of microcystin-LR (MC-LR) on apoptosis based on the endoplasmic reticulum stress (ERS) pathway in mouse liver and kidney, male ICR mice were intraperitoneally injected with 20 μg kg(-1) body weight MC-LR for 21 days, and mRNA and protein levels of ERS special molecules in liver and kidney were analyzed using quantitative real-time PCR and western blotting. MC-LR significantly improved mRNA and protein expression of C/EBP homologous protein (CHOP) and cleaved caspase-12 in liver, whereas it inhibited expression of CHOP and caspase-12 in kidney. MC-LR also induced significant down-regulation of B-cell lymphoma/leukemia-2 (Bcl-2) mRNA expression in liver and weak up-regulation in kidney. These results indicated the involvement of the ERS pathway in MC-LR-induced apoptosis of hepatic cells but not in renal cells of mice. The weight changes and histological damage of liver and kidney were in accordance with the appearance of ERS. Our results indicate that ERS plays an important role in hepatic cell apoptosis induced by MC-LR, and is considered as a new pathway of liver toxicity. Its relative special genes might be considered as potentially new biomarkers used for risk assessment of MC-LR in the environment.
Insights
Microcystin-LR (MC-LR) induces liver cell apoptosis via endoplasmic reticulum stress (ERS), but not in kidney cells. ERS pathway genes may serve as biomarkers for MC-LR risk assessment.
Area of Science:
- Environmental toxicology
- Cellular toxicology
- Molecular biology
Background:
- Microcystin-LR (MC-LR) is a potent cyanotoxin with known hepatotoxicity.
- The mechanisms underlying MC-LR toxicity, particularly apoptosis pathways, require further elucidation.
Purpose of the Study:
- To investigate the role of endoplasmic reticulum stress (ERS) in MC-LR-induced apoptosis in mouse liver and kidney.
- To identify potential molecular biomarkers for MC-LR toxicity.
Main Methods:
- Male ICR mice were injected with MC-LR (20 μg/kg) for 21 days.
- Quantitative real-time PCR and western blotting were used to analyze ERS-related gene and protein expression (CHOP, caspase-12, Bcl-2) in liver and kidney tissues.
Main Results:
- MC-LR significantly upregulated CHOP and cleaved caspase-12, and downregulated Bcl-2 in the liver, indicating ERS involvement in hepatic apoptosis.
- In the kidney, MC-LR inhibited CHOP and caspase-12 expression and weakly upregulated Bcl-2.
- Histological damage and weight changes correlated with ERS markers.
Conclusions:
- Endoplasmic reticulum stress (ERS) is a key pathway in MC-LR-induced hepatic cell apoptosis, representing a novel mechanism of liver toxicity.
- ERS-related genes show potential as biomarkers for environmental risk assessment of MC-LR.
