miR-328 has been shown to target the ABCG2 gene in breast cancer cells and suppress its expression.[30] ABCG2 is one of the ABC transporter proteins that excrete the bile out of liver cells and are expressed on, but not limited to, liver cells, biliary epithelial cells and intestinal epithelial cells.[31, 32] As the bile ducts are exposed to harmful compounds at a high concentration in the bile, this ABCG2 protein expressed on the biliary epithelium is considered to play a protective role by preventing these harmful compounds from penetrating into the bile duct.[33] Thus, the increased expression of miR-328 may negatively

regulate the expression of the ABCG2 gene and thereby make the biliary epithelium vulnerable to injury. It has also been suggested that the activation of auto-reactive

T cells due to molecular Raf targets homology following Escherichia coli infection may be involved in the pathogenesis of PBC.[34] The possibility cannot be ruled out that miR-328 plays a role in the establishment of microbial infection by suppressing the function of ABCG2 protein in intestinal epithelial cells. With no previous study investigating the involvement selleck chemical of ABCG2 in PBC, this issue is worth investigating in future studies. In the evaluation of the relationship between the expression of other miRNAs and clinical test parameters related to PBC, AIH and PBC-AIH overlap syndrome, positive correlations were found between miR-16 expression and GGT and ALP levels, and between miR-26a expression and GGT levels in PBC patients. The expressions of these miRNAs were comparable to those in healthy volunteers. Interestingly, while expression of miR-16 was positively correlated with GGT and ALP levels, parameters considered

to reflect the disease activity of PBC, expression of miR-16 in PBMCs of patients with rheumatoid arthritis (RA) has also been shown to correlate with check details RA activity.[7] Given the decreased expression of miR-26a in the liver tissue of PBC patients as reported previously,[14] further studies are needed to examine the expression pattern of miRNAs in liver tissue. In non-autoimmune liver diseases, various miRNAs exhibiting a significant increase or decrease in liver tissue and plasma samples have been identified. While only eight miRNAs were tested in this study, in a previous study aimed at identifying miRNAs expressed at significantly different levels in patients with non-autoimmune liver diseases compared to healthy individuals, an increased expression of miR-155 was observed in the liver tissue of hepatitis C patients and was considered to be involved in B cell differentiation.[35] Increased expression of miR-146a has also been observed in HepG2 cells infected with hepatitis B, and this was considered to be due to an inflammatory reaction to viral infection.