Fig. 11
Schematic representation of differently expressed genes after AQP4-IgG and active human complement treatment. Differently expressed genes observed in this study are highlighted in red. Grey elements were not investigated in the study. Binding of AQP4-IgG to AQP4 on U-87MG-AQP4-ECFP, primary human astrocytes, or on rat astrocytes enables complement C1q initiation of the classical complement cascade, resulting in the terminal complement complex (TCC). Moreover, the alternative complement pathway and cellular stress are induced. Differently expressed genes are primarily involved in interleukin (IL)-6 and nuclear factor kappa B (NF-κB) activation. AQP4, aquaporin-4; ATF-3, activating transcription factor-3; CEBPB, CCAAT/enhancer-binding protein beta; ERK, extracellular-signal regulated kinase; IRAK2, interleukin-1 receptor-associated kinase 2; IRF1, interferon regulatory factor-1; Jak, Janus kinase; JNK, c-jun N-terminal kinases; JUNB, transcription factor jun-B; MAPK, mitogen-activated protein kinase; NFKB2, NF-κB subunit 2; NFKBIA, NF-κB inhibitor alpha; NFKBIZ, NF-κB inhibitor zeta; NR4A2, nuclear receptor 4A2; P, phosphorylation; PI3K, phosphoinositide 3-kinase; STAT3, signal transducers and activators of transcription-3; Th, T helper; TLR, toll like receptor; TNFR, tumor necrosis factor receptor; PTX-3, pentraxin-3; Ub, ubiquitin. Created in BioRender. Brandl, S. (2025) https://BioRender.com/1x2unnn.
