Liver sinusoidal endothelial cells (LSECs) play a critical role in sensing systemic and/or liver iron levels and release bone morphogenetic proteins (BMPs) that control hepcidin levels in hepatocytes. Our previous results demonstrated that iron-dependent Bmp6 induction in LSECs requires component(s) of the hepatocyte secretome (PMID: 36187873), but the exact mechanism(s) of how iron controls BMP6 levels remains unclear.
Here we show that LSECs in iron-loaded Fpn(C326S) mice show activated PI3K-AKT and MAPK-ERK1/2 signaling pathways. Likewise, primary LSECs cultured in the presence of hepatocyte-conditioned medium with iron show increased phospho-ERK and phospho-AKT levels. Importantly, pretreatment of LSECs with MAPK signaling inhibitors targeting RAF, MEK1/2 and ERK1/2 (Raf265, U0126 and Ulixertinib, respectively), but not with the PI3K inhibitor Wortmannin, attenuated iron-induced Bmp6 expression under hepatocyte-conditioned medium, suggesting the involvement of the ERK1/2 pathway in iron-mediated Bmp6 control. Interestingly, the iron-induced Bmp6 response was only completely abolished when the ERK1/2 pathway was inhibited together with the Nrf2 pathway, suggesting a collaborative function of the ERK1/2 and Nrf2 pathways in controlling BMP6 levels.
Nrf2 is activated by pro-oxidant cellular states. Consistently, we show that H2O2 treatment of LSECs induces Bmp6 mRNA expression, a response that was fully prevented by the ROS scavenger N-Acetyl-L-Cystein (NAC) in the presence of hepatocyte-conditioned medium. By contrast, NAC only attenuated iron-induced Bmp6 mRNA levels, suggesting that iron in LSECs only partially activates Bmp6 by generating oxidative stress. Additional experiments are ongoing to evaluate how the ERK1/2 and Nrf2 pathways interact in controlling the iron sensing process in LSECs.