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Chronic liver diseases, including cancer, are characterized by inflammation and elevated serum ferritin (SF). However, the causal-relationship remains unclear. This study used primary rat hepatic stellate cells (HSC) as a model to investigate effects of physiological SF concentrations (10, 100 and 1000 pM) because HSCs play a central role in the development and progression of liver fibrosis. Physiological concentrations of SF, either horse SF or human serum, induced pro-inflammatory cytokine IL1β, IL6 and TNFα secretion in rat activated HSCs (all p&lt;0.05). By contrast, treatment did not alter activation marker αSMA expression. The presence of SF markedly enhanced expression of Grp78 mRNA (p&lt;0.01). Furthermore, transient knock down of Grp78 by endotoxin EGF- SubA abolished SF-induced IL1β and TNFα secretion in activated HSCs (all p&lt;0.05). In conclusion, our results showed that at physiological concentrations SF functions as a pro-inflammatory mediator in primary rat HSCs. We also provide a molecular basis for the action of SF and identified Grp78-associated ER stress pathways as a novel potential therapeutic target for resolution of fibrosis and possible prevention of liver cancer.

asian pacific journal of cancer prevention

Transient Knock Down of Grp78 Reveals Roles in Serum Ferritin Mediated Pro-inflammatory Cytokine Secretion in Rat Primary Activated Hepatic Stellate Cells