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Stabilizing Hepatocellular Phenotype Using Optimized Synthetic Surfaces
Published on: September 26, 2014
Mitigation of polystyrene microplastic-induced hepatotoxicity in human hepatobiliary organoids through bile
Peilin Li1, Daisuke Miyamoto2, Tomohiko Adachi2
1Department of Surgery, Nagasaki University Graduate School of Biomedical Sciences, 1-7-1 Sakamoto, Nagasaki 852-8102, Japan; Department of Surgery, Guangzhou First People's Hospital, School of Medicine, South China University of Technology, Guangzhou, Guangdong, China.
Background & Aims:
Polystyrene microplastics (PS-MPs) are pervasive in our daily life and can be ingested by the human body through bioaccumulation, causing organ damage, especially liver damage. However, the effect of PS-MPs bioaccumulation on human hepatotoxicity and their metabolism remains unclear. Recent studies have demonstrated that PS-MPs cause lipid and bile acid metabolism disorders. The human hepatobiliary organoids (HBOs) regenerated from chemically induced liver progenitor cells converted by mature hepatocytes and the bile duct provides a bioengineering model for liver disease and hepatic metabolism.
Approach & Results:
Exposure of HBOs to PS-MPs with a diameter of 1 µm for 48 h causes hepatotoxicity, hepatocyte damage, and changes in bile acid metabolism. PS-MPs could be accumulated into the bile ducts of HBOs, which can be promoted by ursodeoxycholic acid, increasing bile flow and volume by activating the bile transporter of BSEP in a dose-dependent manner along with MRP-2. The accumulation of PS-MPs in the bile duct was able to be inhibited by the bile transporter inhibitor of troglitazone that could inhibit the transporters of BSEP and MRP-2, which increased the hepatotoxicity caused by PS-MPs.
Conclusions:
This study provides insights into the metabolic pathways of PS-MPs in the liver and suggests potential therapeutic strategies to reduce MP-induced liver damage.
Insights
Polystyrene microplastics (PS-MPs) accumulate in the liver, causing damage and altering bile acid metabolism. Ursodeoxycholic acid promotes PS-MP accumulation, while troglitazone inhibits it, offering potential therapeutic insights.
Area of Science:
- Environmental Health
- Toxicology
- Hepatology
Background:
- Polystyrene microplastics (PS-MPs) are ubiquitous environmental contaminants.
- PS-MP ingestion and bioaccumulation can lead to human organ damage, particularly liver damage.
- The precise impact of PS-MPs on human hepatotoxicity and their metabolic fate remains largely unknown.
- Emerging evidence suggests PS-MPs disrupt lipid and bile acid metabolism.
Purpose of the Study:
- To investigate the effects of PS-MP bioaccumulation on human hepatotoxicity.
- To elucidate the metabolic pathways of PS-MPs within the liver.
- To explore potential therapeutic strategies for mitigating PS-MP-induced liver injury.
Main Methods:
- Utilized human hepatobiliary organoids (HBOs) as a bioengineered model for liver disease and metabolism.
- Exposed HBOs to 1 µm PS-MPs for 48 hours.
- Investigated the role of bile transporters (BSEP, MRP-2) and their modulators (ursodeoxycholic acid, troglitazone) in PS-MP accumulation and toxicity.
Main Results:
- PS-MP exposure induced hepatotoxicity, hepatocyte damage, and altered bile acid metabolism in HBOs.
- PS-MPs accumulated within the bile ducts of HBOs.
- Ursodeoxycholic acid enhanced PS-MP accumulation and bile flow by activating BSEP and MRP-2.
- Troglitazone, a bile transporter inhibitor, blocked PS-MP accumulation but exacerbated PS-MP-induced hepatotoxicity.
Conclusions:
- This study elucidates the mechanisms of PS-MP accumulation and toxicity in the liver using HBOs.
- Findings highlight the critical role of bile transporters in PS-MP hepatic disposition.
- The study suggests that modulating bile transporter activity could be a potential therapeutic strategy for PS-MP-induced liver damage.
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