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. Author manuscript; available in PMC: 2020 Aug 1.
Published in final edited form as: Exp Neurol. 2019 May 10;318:244–250. doi: 10.1016/j.expneurol.2019.05.003

Figure 7.

Figure 7.

Schematic for hemin clearance by microglia/macrophages following ICH. Hemolysis after ICH causes the release of hemoglobin and hemin. The oxidative stress that can be caused by hemin is reduced by binding to hemopexin (Hpx) which is upregulated after ICH as shown by the current study. In addition, the hemin/Hpx complex is taken up into microglia/macrophages via CD91-mediated endocytosis. CD91 is also upregulated in brain after ICH as shown in the current study. Within microglia/macrophages, hemin is degraded into iron, carbon monoxide (CO) and bilverdin by heme oxygenase-1 (HO-1). Iron is chelated by ferritin to prevent iron-induced oxidative stress. Both HO-1 and ferritin are upregulated after ICH. Hemin increasing their expression by binding to Bach-1, a transcription factor that normally represses the expression of these proteins.