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. Author manuscript; available in PMC: 2024 Feb 1.
Published in final edited form as: Kidney Int. 2022 Oct 28;103(2):331–342. doi: 10.1016/j.kint.2022.09.025

Figure 12. Melanocortin 1 receptor (MC1R) signaling mitigates proinflammatory M1 activation and facilitates the anti-inflammatory M2 polarization of macrophages via repression of nuclear factor (NFκB) activation.

Figure 12.

(a) A schematic diagram depicts the preparation of bone marrow-derived macrophages (BMM) from bone marrow-derived cells (BMDC) isolated from wild-type (WT) or e/e (MC1R-null) mice. (b) BMM cells were primed with a mix of lipopolysaccharide (LPS;100ng/mL) and interferon-γ (IFN-γ; 50ng/mL) in the presence or absence of MC1R agonist MS05 (custom-made peptide, GL Biochem; 10−7M) or pyrrolidine dithiocarbamate (PDTC; 2.5μM). Representative immunoblots show expression of diverse proteins, as well as actin or β-tubulin, which served as loading controls. GM-CSF, granulocyte-macrophage colony-stimulating factor; IL, interleukin; iNOS, inducible nitric oxide synthase; MR, mannose receptor.