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- <i>SLC16A1</i> (1) (remove)
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Membrane monocarboxylate transporter 1 (SLC16A1/MCT1) plays an important role in
hepatocyte homeostasis, as well as drug handling. However, there is no available information
about the impact of liver pathology on the transporter levels and function. The study was aimed to
quantify SLC16A1 mRNA (qRT-PCR) and MCT1 protein abundance (liquid chromatography–tandem
mass spectrometry (LC¬¬–MS/MS)) in the livers of patients diagnosed, according to the standard
clinical criteria, with hepatitis C, primary biliary cirrhosis, primary sclerosing hepatitis, alcoholic liver
disease (ALD), and autoimmune hepatitis. The stage of liver dysfunction was classified according to
Child–Pugh score. Downregulation of SLC16A1/MCT1 levels was observed in all liver pathology
states, significantly for ALD. The progression of liver dysfunction, from Child–Pugh class A to C,
involved the gradual decline in SLC16A1 mRNA and MCT1 protein abundance, reaching a clinically
significant decrease in class C livers. Reduced levels of MCT1 were associated with significant
intracellular lactate accumulation. The MCT1 transcript and protein did not demonstrate significant
correlations regardless of the liver pathology analyzed, as well as the disease stage, suggesting
posttranscriptional regulation, and several microRNAs were found as potential regulators of MCT1
abundance. MCT1 membrane immunolocalization without cytoplasmic retention was observed in all
studied liver pathologies. Overall, the study demonstrates that SLC16A1/MCT1 is involved in liver
pathology, especially in ALD