Macrophage migration inhibitory factor mediates skin aging via CD74 : Insights from single-cell and bulk RNA sequencing data

Copyright © 2024 Elsevier Inc. All rights reserved.

Bibliographische Detailangaben
Veröffentlicht in:Clinical immunology (Orlando, Fla.). - 1999. - 263(2024) vom: 31. Juni, Seite 110199
1. Verfasser: Wu, Songjiang (VerfasserIn)
Weitere Verfasser: Ouyang, Yujie, Hu, Yibo, Jiang, Ling, Fu, Chuhan, Lei, Li, Zhang, Yushan, Guo, Haoran, Huang, Jinhua, Chen, Jing, Zeng, Qinghai
Format: Online-Aufsatz
Sprache:English
Veröffentlicht: 2024
Zugriff auf das übergeordnete Werk:Clinical immunology (Orlando, Fla.)
Schlagworte:Journal Article CD74 Fibroblast MIF Peroxisome proliferation activator receptor γ Skin aging Antigens, Differentiation, B-Lymphocyte Histocompatibility Antigens Class II Intramolecular Oxidoreductases EC 5.3.- mehr... invariant chain Macrophage Migration-Inhibitory Factors MIF protein, human EC 5.3.2.1 PPAR gamma
Beschreibung
Zusammenfassung:Copyright © 2024 Elsevier Inc. All rights reserved.
Cell-cell communication is crucial for regulating signaling and cellular function. However, the precise cellular and molecular changes remain poorly understood in skin aging. Based on single-cell and bulk RNA data, we explored the role of cell-cell ligand-receptor interaction in skin aging. We found that the macrophage migration inhibitory factor (MIF)/CD74 ligand-receptor complex was significantly upregulatedin aged skin, showing the predominant paracrine effect of keratinocytes on fibroblasts. Enrichment analysis and in vitro experiment revealed a close association of the activation of the MIF/CD74 with inflammatory pathways and immune response. Mechanistically, MIF/CD74 could significantly inhibit PPARγ protein, which thus significantly increased the degree of fibroblast senescence, and significantly up-regulated the expression of senescence-associated secretory phenotype (SASP) factors and FOS gene. Therefore, our study reveals that MIF/CD74 inhibits the activation of the PPAR signaling pathway, subsequently inducing the production of SASP factors and the upregulation of FOS expression, ultimately accelerating fibroblast senescence
Beschreibung:Date Completed 17.05.2024
Date Revised 22.08.2024
published: Print-Electronic
Citation Status MEDLINE
ISSN:1521-7035
DOI:10.1016/j.clim.2024.110199