Journal: Redox Biology

Article Title: Macrophage AMPK activated by oxidative stress drives profibrotic crosstalk with tubular cells to accelerate renal fibrosis after ischemic and reperfusion injury

doi: 10.1016/j.redox.2025.104002

Figure Lengend Snippet: Arg1 + MMP12 + macrophage-derived TWEAK licenses PDGFB production in fibroTECs via Fn14 signaling. (A) Ligand-receptor communication analysis between different cell types in IRI kidneys. (B) The major incoming signaling of different cell types. (C) Bubble plots showing the expression of specific ligand-receptor pairs in the interaction between myeloid cell subsets and TEC subsets. (D) Bubble plots showing the expression of specific ligand-receptor pairs in the interaction between TEC subsets and myeloid cell subsets. (E, F) WT/AMPKα1 −/− BMDMs were treated with IL-4 and IL-13, and the expression levels of Arg 1 , Mmp12 , and Tnfsf12 were analyzed by qPCR (n = 5). (G, H) TCMK-1 cells were treated with CM from IL-4 and IL-13-stimulated WT/AMPKα1 −/− BMDMs. The expression of Pdgfb , Cxcl1 , and Egfr in TCMK-1 cells was analyzed by qPCR (n = 5). (I, J) TCMK-1 cells were treated with CM from IL-4 and IL-13-stimulated WT/AMPKα1 −/− BMDMs or together with recombinant TWEAK (rTWEAK). The expression of Pdgfb in TCMK-1 cells was analyzed by qPCR (n = 5). (K, L) TCMK-1 cells were treated with rTWEAK or rTWEAK and an Fn14 inhibitor. The expression of Pdgfb in TCMK-1 cells was detected by qPCR (n = 5). (M) Immunoblots and quantification of IKK-β and nuclear NF-κB p65 in TCMK-1 cells treated with PBS or rTWEAK (n = 3). The results represent mean ± SEM. ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001.

Article Snippet: To examine the role of the TWEAK-Fn14 axis, cells were treated with recombinant TWEAK (MCE, HY-P7309, 100 ng/ml) and the Fn14 inhibitor, L524-0366 (Sigma, 509374, 10 μM).

Techniques: Derivative Assay, Expressing, Recombinant, Western Blot