Narrow-band UVB radiation triggers diverse changes in the gene expression and induces the accumulation of M1 macrophages in human skin.

Human skin Transcriptome Ultraviolet UVB radiation

Journal

Journal of photochemistry and photobiology. B, Biology
ISSN: 1873-2682
Titre abrégé: J Photochem Photobiol B
Pays: Switzerland
ID NLM: 8804966

Informations de publication

Date de publication:
06 Mar 2024
Historique:
received: 26 01 2024
revised: 22 02 2024
accepted: 05 03 2024
medline: 10 3 2024
pubmed: 10 3 2024
entrez: 9 3 2024
Statut: aheadofprint

Résumé

The underlying molecular mechanisms that determine the biological effects of UVB radiation exposure on human skin are still only partially comprehended. Our goal is to examine the human skin transcriptome and related molecular mechanisms following a single exposure to UVB in the morning versus evening. We exposed 20 volunteer females to four-fold standard erythema doses (SED4) of narrow-band UVB (309-313 nm) in the morning or evening and studied skin transcriptome 24 h after the exposure. We performed enrichment analyses of gene pathways, predicted changes in skin cell composition using cellular deconvolution, and correlated cell proportions with gene expression. In the skin transcriptome, UVB exposure yielded 1384 differentially expressed genes (DEGs) in the morning and 1295 DEGs in the evening, of which the most statistically significant DEGs enhanced proteasome and spliceosome pathways. Unexposed control samples showed difference by 321 DEGs in the morning vs evening, which was related to differences in genes associated with the circadian rhythm. After the UVB exposure, the fraction of proinflammatory M1 macrophages was significantly increased at both timepoints, and this increase was positively correlated with pathways on Myc targets and mTORC1 signaling. In the evening, the skin clinical erythema was more severe and had stronger positive correlation with the number of M1 macrophages than in the morning after UVB exposure. The fractions of myeloid and plasmacytoid dendritic cells and CD8 T cells were significantly decreased in the morning but not in the evening. NB-UVB-exposure causes changes in skin transcriptome, inhibiting cell division, and promoting proteasome activity and repair responses, both in the morning and in the evening. Inflammatory M1 macrophages may drive the UV-induced skin responses by exacerbating inflammation and erythema. These findings highlight how the same UVB exposure influences skin responses differently in morning versus evening and presents a possible explanation to the differences in gene expression in the skin after UVB irradiation at these two timepoints.

Sections du résumé

BACKGROUND BACKGROUND
The underlying molecular mechanisms that determine the biological effects of UVB radiation exposure on human skin are still only partially comprehended.
OBJECTIVES OBJECTIVE
Our goal is to examine the human skin transcriptome and related molecular mechanisms following a single exposure to UVB in the morning versus evening.
METHODS METHODS
We exposed 20 volunteer females to four-fold standard erythema doses (SED4) of narrow-band UVB (309-313 nm) in the morning or evening and studied skin transcriptome 24 h after the exposure. We performed enrichment analyses of gene pathways, predicted changes in skin cell composition using cellular deconvolution, and correlated cell proportions with gene expression.
RESULTS RESULTS
In the skin transcriptome, UVB exposure yielded 1384 differentially expressed genes (DEGs) in the morning and 1295 DEGs in the evening, of which the most statistically significant DEGs enhanced proteasome and spliceosome pathways. Unexposed control samples showed difference by 321 DEGs in the morning vs evening, which was related to differences in genes associated with the circadian rhythm. After the UVB exposure, the fraction of proinflammatory M1 macrophages was significantly increased at both timepoints, and this increase was positively correlated with pathways on Myc targets and mTORC1 signaling. In the evening, the skin clinical erythema was more severe and had stronger positive correlation with the number of M1 macrophages than in the morning after UVB exposure. The fractions of myeloid and plasmacytoid dendritic cells and CD8 T cells were significantly decreased in the morning but not in the evening.
CONCLUSIONS CONCLUSIONS
NB-UVB-exposure causes changes in skin transcriptome, inhibiting cell division, and promoting proteasome activity and repair responses, both in the morning and in the evening. Inflammatory M1 macrophages may drive the UV-induced skin responses by exacerbating inflammation and erythema. These findings highlight how the same UVB exposure influences skin responses differently in morning versus evening and presents a possible explanation to the differences in gene expression in the skin after UVB irradiation at these two timepoints.

Identifiants

pubmed: 38460430
pii: S1011-1344(24)00047-2
doi: 10.1016/j.jphotobiol.2024.112887
pii:
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

112887

Informations de copyright

Copyright © 2023. Published by Elsevier B.V.

Déclaration de conflit d'intérêts

Declaration of competing interest The authors declare the following financial interests/personal relationships which may be considered as potential competing interests: Erna Snellman reports financial support was provided by Expert Responsibility Area of Tampere University Hospital. If there are other authors, they declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.

Auteurs

Piia Karisola (P)

Faculty of Medicine, Human Microbiome Research Program, University of Helsinki, Finland. Electronic address: piia.karisola@helsinki.fi.

Veera Nikkola (V)

Tampere University, Faculty of Medicine and Health Technology, Department of Dermatology and Venereology, Tampere, Finland.

Heli Joronen (H)

Tampere University, Faculty of Medicine and Health Technology, Department of Dermatology and Venereology, Tampere, Finland; Päijät-Häme Social and Health Care Group, Department of Dermatology and Allergology, Lahti, Finland. Electronic address: Heli.Joronen@pshp.fi.

Lasse Ylianttila (L)

Radiation and Nuclear Safety Authority (STUK), Helsinki, Finland. Electronic address: Lasse.Ylianttila@stuk.fi.

Mari Grönroos (M)

Päijät-Häme Social and Health Care Group, Department of Dermatology and Allergology, Lahti, Finland. Electronic address: mari.gronroos@outlook.com.

Timo Partonen (T)

Finnish Institute for Health and Welfare, Department of Public Health and Welfare, Finland. Electronic address: timo.partonen@thl.fi.

Erna Snellman (E)

Tampere University, Faculty of Medicine and Health Technology, Department of Dermatology and Venereology, Tampere, Finland. Electronic address: erna.snellman@tuni.fi.

Harri Alenius (H)

Faculty of Medicine, Human Microbiome Research Program, University of Helsinki, Finland; Institute of Environmental Medicine, Karolinska Institute, Stockholm, Sweden. Electronic address: harri.alenius@helsinki.fi.

Classifications MeSH