Expression and significance of mitochondrial transcription factor A in hepatocytes of infants with cholestatic jaundice

Abstract

Objective To investigate the expression of mitochondrial transcription factor A (mtTFA) in hepatocytes of infants with cholestatic jaundice and explore the possible regulatory mechanism. Methods The liver samples and clinical data of the infants with cholestatic jaundice were collected; The cholestatic model of glycochenodeoxycholic acid (GCDCA)-induced human normal hepatocyte (L02) was constructed. HE staining was used to detect morphological changes of the liver tissues. Real-time PCR and qRT-PCR were adopted to detect the mitochondral DNA (mtDNA) copy number and transcription level, and mRNA levels of mtTFA and silent mating type information regulator 2 homolog 1 (SIRT1) pathway-related genes. Western blotting was used to measure the protein levels of mtTFA and SIRT1 pathway-related proteins. Results Clinical statistics presented that liver function of the jaundice group was significantly lower than that of control group (P 0.05). Treatment with SIRT1 agonist SRT1720 resulted in increased expression level of mtTFA protein (P < 0.05). Conclusion The expression level of mtTFA is obviously decreased in hepatocytes of infants with cholestatic jaundice, and SIRT1 signaling pathway may play a regulatory role in its expression.

Keywords

• nfants
• cholestasis
• hepatocytes
• mitochondrial transcription factor a
• silent mating type information regulator 2 homolog 1