1. Academic Validation
  2. Interleukin-24: A molecular mediator of particulate matter's impact on skin aging

Interleukin-24: A molecular mediator of particulate matter's impact on skin aging

  • Ecotoxicol Environ Saf. 2024 Jul 18:282:116738. doi: 10.1016/j.ecoenv.2024.116738.
Seol Hwa Seong 1 Ji Young Kim 1 Sung Hee Kim 1 Joohee Lee 1 Eun Jung Lee 1 Yu Jeong Bae 1 Sujin Park 1 Il Joo Kwon 1 Sei-Mee Yoon 2 Jinu Lee 3 Tae-Gyun Kim 4 Sang Ho Oh 5
Affiliations

Affiliations

  • 1 Department of Dermatology and Cutaneous Biology Research Institute, Severance Hospital, Yonsei University College of Medicine, Seoul, South Korea.
  • 2 College of Pharmacy, Institute of Pharmaceutical Sciences, Yonsei University, 85 Songdogwahakro, Yeonsu-gu, Incheon, South Korea.
  • 3 College of Pharmacy, Institute of Pharmaceutical Sciences, Yonsei University, 85 Songdogwahakro, Yeonsu-gu, Incheon, South Korea. Electronic address: jinulee@yonsei.ac.kr.
  • 4 Department of Dermatology and Cutaneous Biology Research Institute, Severance Hospital, Yonsei University College of Medicine, Seoul, South Korea. Electronic address: tgmed83@yuhs.ac.
  • 5 Department of Dermatology and Cutaneous Biology Research Institute, Severance Hospital, Yonsei University College of Medicine, Seoul, South Korea. Electronic address: oddung93@yuhs.ac.
Abstract

Air pollution, a global health concern, has been associated with adverse effects on human health. In particular, particulate matter (PM), which is a major contributor to air pollution, impacts various organ systems including the skins. In fact, PM has been suggested as a culprit for accelerating skin aging and pigmentation. In this study, using single-cell RNA Sequencing, IL-24 was found to be highly upregulated among the differentially expressed genes commonly altered in keratinocytes and fibroblasts of ex vivo skins exposed to PM. It was verified that PM exposure triggered the expression of IL-24 in keratinocytes, which subsequently led to a decrease in type I procollagen expression and an increase in MMP1 expression in fibroblasts. Furthermore, long-term treatment of IL-24 induced cellular senescence in fibroblasts. Through high-throughput screening, we identified chemical compounds that inhibit the IL-24-STAT3 signaling pathway, with lovastatin being the chosen candidate. Lovastatin not only effectively reduced the expression of IL24 induced by PM in keratinocytes but also exhibited a capacity to restore the decrease in type I procollagen and the increase in MMP1 caused by IL-24 in fibroblasts. This study provides insights into the significance of IL-24, illuminating mechanisms behind PM-induced skin aging, and proposes IL-24 as a promising target to mitigate PM-associated skin aging.

Keywords

Interleukin-24; Lovastatin; MMP1; Particulate matter; Skin aging.

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