Hepatic stellate cells (HSCs) are liver-resident cells best known for their role in vitamin A (retinol) storage under physiological conditions, whereby retinyl esters are stored in characteristic large lipid droplets. Upon liver injury, HSCs activate into myofibroblast-like cells, a key process in the onset of liver fibrosis. Upon activation, HSCs lose their retinyl esters and secrete both extracellular matrix components and signaling molecules.
Comprehensive characterization of the lipidomes of primary HSCs during activation revealed a two stage process in which lysosomes play an important role. Metabolic labeling revealed the presence of two metabolically different lipid droplets (LDs): an original pool of preexisting/“original” LDs and a transient and rapidly recycling pool of “new” LDs. These two LD pools of lipid droplets are under control of different cellular machineries with surprising divergent as well as convergent
mechanisms.

Bio:
Bernd Helms studied Biochemistry at Utrecht University (The Netherlands) and graduated on intracellular lipid transport mechanisms. After his postdoctoral research with Dr. James E. Rothman (Nobel prize laureate 2013, USA) focusing on intracellular protein transport mechanisms, he became junior group leader at Heidelberg University (Germany). Here, Bernd developed his current research interest in membrane dynamics. In 2002 Bernd became full professor at Utrecht University, where his research focuses around hepatic stellate cells that play a role in the onset of liver inflammation and fibrosis. Lipid and protein transport processes, as well as lipid storage in lipid droplets, play an important role in the transition from quiescent to activated hepatic stellate cells. We aim to apply our lipid and hepatic stellate cell research to pathophysiological research in fatty liver diseases, ranging from NAFLD/MASLD and NASH/MASH to hepatocellular carcinoma.