Journal: Cell Death Discovery

Article Title: IL‑1 receptor antagonism attenuates renal fibrosis via RNF182‑driven MFN2 destabilization and mitochondrial dysfunction

doi: 10.1038/s41420-025-02929-4

Figure Lengend Snippet: In the context of kidney injury, pro-inflammatory stimuli upregulate the expression of the Interleukin-1 Receptor (IL-1R) and its downstream effector, TGF-β1, in renal tubular epithelial cells. This leads to increased expression of the E3 ubiquitin ligase RNF182. RNF182, in turn, forms a complex with the mitochondrial fusion protein Mitofusin 2 (MFN2), targeting it for ubiquitination and subsequent proteasomal degradation. The depletion of MFN2 results in mitochondrial dysfunction, characterized by excessive reactive oxygen species (ROS) production and reduced ATP synthesis, which drives the progression of renal fibrosis. Therapeutic administration of recombinant human IL-1 receptor antagonist (rhIL-1Ra) blocks IL-1R signaling. This intervention suppresses the downstream upregulation of RNF182, thereby reducing MFN2 ubiquitination and degradation. The stabilization of MFN2 protein preserves mitochondrial function, mitigates oxidative stress, and restores cellular energy production, ultimately exerting a potent anti-fibrotic effect and protecting kidney tissue.

Article Snippet: Cells grown on coverslips were fixed with 4% PFA for 15 min, permeabilized with 0.2% Triton X-100 in PBS for 10 min, and blocked with 5% BSA in PBS for 1 h. Cells were incubated with primary antibodies against IL-1R (R&D Systems, Cat# AF269, 1:100 dilution) overnight at 4 °C.

Techniques: Expressing, Ubiquitin Proteomics, Recombinant

Journal: Reproduction

Article Title: Stable inhibition of interleukin 1 receptor type II in Ishikawa cells augments secretion of matrix metalloproteinases: possible role in endometriosis pathophysiology

doi: 10.1530/rep-06-0377

Figure Lengend Snippet: Figure 2 Immunofluorescence analysis of IL1R1, IL1R2, and IL1RAcP expression in non-transfected Ishikawa cells (NT) and E03, E11, A08, and A17 clones. Note the com- parable intensity of IL1R1 and IL1RAcP immunofluorescent signals in NT, E03, and E11 clones, and the marked decline in IL1R2 immunofluorescent signal in A08 and A17 clones. No immunofluorescence was observedinnegativecontrols(c)in theabsence of primary antibodies (objective !40).

Article Snippet: Membranes were incubated for 3 h at room temperature with a polyclonal goat anti-human IL1R1 (R&D Systems; www.reproduction-online.org 2 mg/ml in blocking solution), a polyclonal goat anti-human IL1R2 (R&D Systems; 2 mg/ml in blocking solution), or a polyclonal goat anti-human IL1RAcP (R&D Systems; 2 mg/ml in blocking solution).

Techniques: Expressing, Transfection, Clone Assay

Journal: Reproduction

Article Title: Stable inhibition of interleukin 1 receptor type II in Ishikawa cells augments secretion of matrix metalloproteinases: possible role in endometriosis pathophysiology

doi: 10.1530/rep-06-0377

Figure Lengend Snippet: Figure 3 Representative Western blot analysis of IL1R1 (A), IL1R2 (B), and IL1RAcP (C) expression in non-transfected Ishikawa cells (NT) and E03, E11, A08, and A17 clones. Equal amounts of proteins were subjected to SDS-PAGE analysis and Western blotting. Recombinant IL1R1, IL1R2, and IL1RAcP proteins were taken as controls (rR). Blotting with anti-tubulin antibody demonstrates equal protein loading. Note the reduced intensity of IL1R2 bands corresponding to either the membrane-bound or the soluble forms of the receptor, when compared with NT cells, and the absence of noticeable change in IL1R1 and IL1RAcP expression; mb, membrane-bound; s, soluble.

Article Snippet: Membranes were incubated for 3 h at room temperature with a polyclonal goat anti-human IL1R1 (R&D Systems; www.reproduction-online.org 2 mg/ml in blocking solution), a polyclonal goat anti-human IL1R2 (R&D Systems; 2 mg/ml in blocking solution), or a polyclonal goat anti-human IL1RAcP (R&D Systems; 2 mg/ml in blocking solution).

Techniques: Western Blot, Expressing, Transfection, Clone Assay, SDS Page, Recombinant, Membrane