Caspase Inhibition Modulates Monocyte-Derived Macrophage Polarization in Damaged Tissues.

Publisher: MDPI Country of Publication: Switzerland NLM ID: 101092791 Publication Model: Electronic Cited Medium: Internet ISSN: 1422-0067 (Electronic) Linking ISSN: 14220067 NLM ISO Abbreviation: Int J Mol Sci Subsets: MEDLINE

Original Publication: Basel, Switzerland : MDPI, [2000-

Macrophage Colony-Stimulating Factor*/metabolism ; Caspases*/metabolism; Humans ; Animals ; Mice ; Caspase 7/metabolism ; Reactive Oxygen Species/metabolism ; Macrophages/metabolism ; NADPH Oxidases/metabolism ; Monocytes/metabolism

Circulating monocytes are recruited in damaged tissues to generate macrophages that modulate disease progression. Colony-stimulating factor-1 (CSF-1) promotes the generation of monocyte-derived macrophages, which involves caspase activation. Here, we demonstrate that activated caspase-3 and caspase-7 are located to the vicinity of the mitochondria in CSF1-treated human monocytes. Active caspase-7 cleaves p47 ^PHOX at aspartate 34, which promotes the formation of the NADPH (nicotinamide adenine dinucleotide phosphate) oxidase complex NOX2 and the production of cytosolic superoxide anions. Monocyte response to CSF-1 is altered in patients with a chronic granulomatous disease, which are constitutively defective in NOX2. Both caspase-7 down-regulation and radical oxygen species scavenging decrease the migration of CSF-1-induced macrophages. Inhibition or deletion of caspases prevents the development of lung fibrosis in mice exposed to bleomycin. Altogether, a non-conventional pathway that involves caspases and activates NOX2 is involved in CSF1-driven monocyte differentiation and could be therapeutically targeted to modulate macrophage polarization in damaged tissues.

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Keywords: CSF1; NOX2; caspase; differentiation; lung fibrosis; macrophage

81627-83-0 (Macrophage Colony-Stimulating Factor)
EC 3.4.22.- (Caspase 7)
EC 3.4.22.- (Caspases)
0 (Reactive Oxygen Species)
EC 1.6.3.- (NADPH Oxidases)

Date Created: 20230225 Date Completed: 20230228 Latest Revision: 20230301

20231215

PMC9964254

10.3390/ijms24044151

36835566