ArticleScientific reports2017
AQP3 is regulated by PPARγ and JNK in hepatic stellate cells carrying PNPLA3 I148M.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 18 citations in OpenAlex.
- Aquaporin membrane channels in the hepatobiliary tract: a model of complexity and clinical implications in health and disease.Internal and emergency medicine · 2026Review
- Aquaporins in Biliary Function: Pathophysiological Implications and Therapeutic Targeting.International journal of molecular sciences · 2024Review
- PPAR-γ/NF-kB/AQP3 axis in M2 macrophage orchestrates lung adenocarcinoma progression by upregulating IL-6.Cell death & disease · 2024Article
- Article
- The Role of Metabolic Lipases in the Pathogenesis and Management of Liver Disease.Hepatology (Baltimore, Md.) · 2020Review
- Metabolic regulation of hepatic PNPLA3 expression and severity of liver fibrosis in patients with NASH.Liver international : official journal of the International Association for the Study of the Liver · 2020Article
- Monoacylglycerol Lipase Inhibition Protects From Liver Injury in Mouse Models of Sclerosing Cholangitis.Hepatology (Baltimore, Md.) · 2020Article
- AQP3 Facilitates Proliferation and Adipogenic Differentiation of Porcine Intramuscular Adipocytes.Genes · 2020Article
- Mannosylerythritol lipids ameliorate ultraviolet A-induced aquaporin-3 downregulation by suppressing c-Jun N-terminal kinase phosphorylation in cultured human keratinocytes.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2019Article
- Identification of Phf16 and Pnpla3 as new adipogenic factors regulated by phytochemicals.Journal of cellular biochemistry · 2019Article
- Aquaporin 11-Dependent Inhibition of Proliferation by Deuterium Oxide in Activated Hepatic Stellate Cells.Molecules (Basel, Switzerland) · 2018Article
- Nuclear Receptor Regulation of Aquaglyceroporins in Metabolic Organs.International journal of molecular sciences · 2018Review
- Aquaglyceroporins: Drug Targets for Metabolic Diseases?Frontiers in physiology · 2018Review
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Aquaglyceroporins (AQPs) allow the movement of glycerol that is required for triglyceride formation in hepatic stellate cells (HSC), as key cellular source of fibrogenesis in the liver. The genetic polymorphism I148M of the patatin-like phospholipase domain-containing 3 (PNPLA3) is associated with hepatic steatosis and its progression to steatohepatitis (NASH), fibrosis and cancer. We aimed to explore the role of AQP3 for HSC activation and unveil its potential interactions with PNPLA3. HSC were isolated from human liver, experiments were performed in primary HSC and human HSC line LX2. AQP3 was the only aquaglyceroporin present in HSC and its expression decreased during activation. The PPARγ agonist, rosiglitazone, recovered AQP3 expression also in PNPLA3 I148M carrying HSC. When PNPLA3 was silenced, AQP3 expression increased. In liver sections from patients with NASH, the decreased amount of AQP3 was proportional to the severity of fibrosis and presence of the PNPLA3 I148M variant. In PNPLA3 I148M cells, the blockade of JNK pathway upregulated AQP3 in synergism with PPARγ. In conclusion, we demonstrated profound reduction of AQP3 in HSC carrying the PNPLA3 I148M variant in parallel to decreased PPARγ activation, which could be rescued by rosiglitazone and blockade of JNK.
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