Multi-System-Level Analysis Reveals Differential Expression of Stress Response-Associated Genes in Inflammatory Solar Lentigo

Although the pathogenesis of solar lentigo (SL) involves chronic ultraviolet (UV) exposure, cellular senescence, and upregulated melanogenesis, underlying molecular-level mechanisms associated with SL remain unclear. The aim of this study was to investigate the gene regulatory mechanisms intimately...

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Bibliographic Details
Published in:International journal of molecular sciences 2024-04, Vol.25 (7), p.3973
Main Authors: Jeong, Jisu, Lee, Wonmin, Kim, Ye-Ah, Lee, Yun-Ji, Kim, Sohyun, Shin, Jaeyeon, Choi, Yueun, Kim, Jihan, Lee, Yoonsung, Kim, Man S, Kwon, Soon-Hyo
Format: Article
Language:English
Subjects:
Biotechnology industry
Cellular Senescence
Chemokines
Comparative analysis
Cytokines
Fibroblasts
Gene expression
Genes
Genetic aspects
Genetic transcription
Humans
Hyperplasia
Immunity, Innate
Inflammation
Inflammation - genetics
Lentigo - genetics
Metabolism
Multigene Family
Oxidative stress
Proteins
RNA
Senescence
Skin
Tumor necrosis factor-TNF
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Summary:Although the pathogenesis of solar lentigo (SL) involves chronic ultraviolet (UV) exposure, cellular senescence, and upregulated melanogenesis, underlying molecular-level mechanisms associated with SL remain unclear. The aim of this study was to investigate the gene regulatory mechanisms intimately linked to inflammation in SL. Skin samples from patients with SL with or without histological inflammatory features were obtained. RNA-seq data from the samples were analyzed via multiple analysis approaches, including exploration of core inflammatory gene alterations, identifying functional pathways at both transcription and protein levels, comparison of inflammatory module (gene clusters) activation levels, and analyzing correlations between modules. These analyses disclosed specific core genes implicated in oxidative stress, especially the upregulation of nuclear factor kappa B in the inflammatory SLs, while genes associated with protective mechanisms, such as SLC6A9, were highly expressed in the non-inflammatory SLs. For inflammatory modules, Extracellular Immunity and Mitochondrial Innate Immunity were exclusively upregulated in the inflammatory SL. Analysis of protein-protein interactions revealed the significance of CXCR3 upregulation in the pathogenesis of inflammatory SL. In conclusion, the upregulation of stress response-associated genes and inflammatory pathways in response to UV-induced oxidative stress implies their involvement in the pathogenesis of inflammatory SL.
ISSN:1422-0067
1661-6596
1422-0067
DOI:10.3390/ijms25073973