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. 2022 Dec 9;12:21375. doi: 10.1038/s41598-022-25855-2

Figure 5.

Figure 5

A schematic presentation of the possible role of the NF-κB p65 subunit and the GRO-α/CXCR2 axis in the formation of IA. The first step initiating the formation of IA is the activation of the canonical/classical NF-κB pathway in the arterial bifurcationas as the result of hemodynamic stress. NF-κB activation occurs through the phosphorylation and proteasomal degradation of IκB. An active form of NF-κB p50/p65 heterodimer bind to DNA to function as a transcription factor of pro-inflammatory cytokine genes, including chemokine GRO-α. Secretory chemokine GRO-α, via its CXCR2 receptor, acts as a chemoattractant for leukocytes and increases endothelial cell proliferation, which initiates the formation of IA. As a result of forming IA, also microglia and astrocytes could secrete GRO-α, which in turn enhances leukocyte trafficking and endothelial cell proliferation. CXCR2, C-X-C Motif Chemokine Receptor 2; GRO-α, GRO alpha chemokine/C-X-C motif ligand 1 (CXCL1); IA, intracranial aneurysms; IκB, IkappaB kinase; NF-κB p50, nuclear factor kappa-B p50 subunit; NF-κB p65, nuclear factor kappa-B p65 subunit; NF-κB, nuclear factor kappa-B.