【Report】AJI–Medical Chemistry Laboratory Joint Seminar: Dr. Urushima (Osaka Metropolitan University) talks about hepatic stellate cells

Mikio Nishizawa, M.D., Ph.D., Professor
Medical Chemistry Laboratory, Department of Biomedical Sciences, College of Life Sciences, Project Leader of "Prevention of diabetes mellitus by traditional Asian drugs and foods"

AJI–Medical Chemistry Laboratory Joint Seminar was held at the room (5th floor, BioLink) in Biwako-Kusatsu Campus from 15:00 to 16:00 on October 21, 2022. The plenary speaker is Dr. Hayato Urushima (Lecturer, Department of Anatomy and Regenerative Biology, Graduate School of Medicine, Osaka Metropolitan University) and talked on “Development of drugs that de-activate hepatic stellate cells (HSCs) by focusing liver-specific structures.” He explained about the functions of HSCs and the approach to seek functional foods that prevent liver cirrhosis by suppressing the HSC functions.

Dr. Hayato Urushima

It is well-known that there is close relationship between diabetes mellitus (DM) and hepatic disorders. One among about 10 patients suffering with DM died by hepatic disorders. Indeed, having type 2 DM increases a risk of developing hepatocellular carcinoma. Furthermore, liver cirrhosis is closely relating with hepatocellular carcinoma, and HSCs play an important role in hepatic fibrosis. Collectively, it is considered that DM and obesity facilitate fibrosis in the liver, leading to liver cirrhosis and finally carcinogenesis (i.e., hepatocellular carcinoma).

HSCs are star-shaped mesenchymal cells that are resident in the liver, and their population is only 10% of the total cell number in the liver. Quiescent HSCs store vitamin A (as lipid droplets), which is most part of the whole storage of vitamin A in the body. In response to injury, HSCs are activated (i.e., transdifferentiation into myofibroblasts) to secrete the cytokine TGF-β and the extracellular matrix including collagen and then repair the injured region with them. During chronic hepatitis, HSCs are persistently activated to cause fibrosis, resulting in liver cirrhosis. Because liver cirrhosis is the end-stage of the hepatic disorders, prevention of the development to hepatic fibrosis is clinically essential.

When HSCs are activated, a phenomenon similar to epithelial–mesenchymal transformation, which occurs during carcinogenesis, is observed. Dr. Urushima's group speculated that the activation of HSCs may be blocked when the HSCs are transformed to epithelioid cells. His group has found a few candidate compounds by screening of several thousands of natural and synthetic compounds. There is detailed explanation about this approach in the seminar. Because hepatic fibrosis develops very slowly, it is important to prevent it by paying attention to the daily habits. Dr. Urushima's group investigates other functional foods that suppress the HSC functions. In addition, Dr. Urushima is veterinary doctor and responsible for the animal facility of Osaka Metropolitan University. He gave interesting topics about comparative zoology.

During and after the talk, there was discussion with the audience about the functions of HSCs and the activation mechanism of HSCs. Difficulty to prepare mouse HSCs due to a small population in the liver cells was also discussed in details. The seminar provided fruitful results after intensive discussion. Thank you very much for all the participants in this seminar!

Dr. Urushima delivering a lecture

Attendees for this lecture