Background: Reactive oxygen species generated in the skin by UV irradiation promote photoaging and photocarcinogenesis. The manganese (Mn) superoxide dismutase (SOD) is a primary antioxidant enzyme that crucially contributes to the homeostasis of oxygen radicals within the mitochondria, and thus critically participates in the control of senescence and tumor generation.
Objective: To determine whether repetitive UV-B exposure, as practiced for light hardening during phototherapy for various photodermatoses, can enhance the adaptive antioxidant response by up-regulating MnSOD activity in either the epidermal or the dermal skin compartment.
Design: In vitro experiments to determine MnSOD activity levels in cultured human dermal fibroblasts and epidermal cells (HaCaT cells and primary keratinocytes) at different times after direct UV-B exposure or after incubation of human dermal fibroblasts with supernatants from UV-B-irradiated epidermal cells.
Setting: Photobiological research laboratory in a university dermatology department.
Intervention: Irradiation of cultured human dermal fibroblasts and epidermal cells with UV-B.
Main Outcome Measures: Manganese SOD messenger RNA and activity levels in cultured irradiated or mock-treated skin cells.
Results: No increase in MnSOD activity could be detected in fibroblasts or epidermal cells until 24 hours after UV-B irradiation. However, fibroblasts incubated with supernatants from UV-B-irradiated epidermal cells showed a marked increase in specific MnSOD messenger RNA and activity. Removal of interleukin 1alpha, interleukin 1beta, and tumor necrosis factor alpha from the supernatants led to a significant reduction of MnSOD mRNA in fibroblasts.
Conclusion: Irradiation of the epidermal cells with UV-B induced a release of soluble factors that amplified MnSOD activity in fibroblasts via a paracrine mechanism.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1001/archderm.138.11.1473 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Epidermal stem cell derived exosomes-induced dedifferentiation of myofibroblasts inhibits scarring via the miR-203a-3p/PIK3CA axis.
J Nanobiotechnology
January 2025
Department of Burns, Wound Repair and Reconstruction, First Affiliated Hospital of Sun Yat-Sen University, Guangzhou, Guangdong, 510080, China.
Hypertrophic scar (HS) is a common fibroproliferative disorders with no fully effective treatments. The conversion of fibroblasts to myofibroblasts is known to play a critical role in HS formation, making it essential to identify molecules that promote myofibroblast dedifferentiation and to elucidate their underlying mechanisms. In this study, we used comparative transcriptomics and single-cell sequencing to identify key molecules and pathways that mediate fibrosis and myofibroblast transdifferentiation.
View Article and Find Full Text PDFAnatomical characterization of Semi-arid Bignoniaceae using light and scanning electron microscopy.
BMC Plant Biol
January 2025
Plant Production Department, College of Food and Agricultural Sciences, King Saud University, P.O. Box. 2460, Riyadh, 11451, Saudi Arabia.
Background: The present research work was done to evaluate the anatomical differences among selected species of the family Bignoniaceae, as limited anatomical data is available for this family in Pakistan. Bignoniaceae is a remarkable family for its various medicinal properties and anatomical characterization is an important feature for the identification and classification of plants.
Methodology: In this study, several anatomical structures were examined, including stomata type and shape, leaf epidermis shape, epidermal cell size, and the presence or absence of trichomes and crystals (e.
Triptolide's impact on ACER1 signaling: Inducing autophagy for triple-negative breast cancer suppression.
Pathol Res Pract
January 2025
Clinical Pharmacy & Pharmacology Research Institute, Affiliated Hospital of Guilin Medical University, Guilin 541001, China; Guangxi Key Laboratory of Molecular Medicine in Liver Injury and Repair, Affiliated Hospital of Guilin Medical University, Guilin 541001, China; Guangxi Health Commission Key Laboratory of Basic Research in Sphingolipid Metabolism Related Diseases, the Affiliated Hospital of Guilin Medical University, Guilin 541001, China; China-USA Lipids in Health and Disease Research Center, Guilin Medical University,Guilin 541001, China; Laboratory of Hepatobiliary and Pancreatic Surgery, Affiliated Hospital of Guilin Medical University, Guilin 541001, China. Electronic address:
Given the absence of estrogen receptor (ER), progesterone receptor (PR), and human epidermal growth factor receptor-2 (Her-2) in triple-negative breast cancer (TNBC) cells, the efficacy of targeted therapies is limited. In this study, we uncovered that triptolide (TP) effectively suppresses the migration and invasiveness of MDA-MB-231 cells by activating autophagic pathways. Western blotting analysis revealed that TP significantly reduced the expression levels of p62 protein, while simultaneously markedly increasing the expression levels of LC3B-II, BNIP3, BNIP3L, ATG5, and ULK1 proteins, strongly suggesting an enhancement of autophagic activity in the cells.
View Article and Find Full Text PDFStudy of the role of transmembrane emp24 domain-containing protein 2 in oral squamous cell carcinoma.
J Appl Oral Sci
January 2025
Ningde Hospital Affiliated to Ningde Normal University, Department of Stomatology, Fujian, China.
Objective: This study aimed to investigate the role of transmembrane emp24 domain-containing protein 2 (TMED2) in oral squamous cell carcinoma (OSCC).
Methodology: A bioinformatics analysis was first conducted to explore TMED2 expression in OSCC and its relation with overall survival. The analysis results were further verified by assessing TMED2 expression levels in human normal oral keratinocyte cells and human OSCC cell lines using quantitative real-time polymerase chain reaction and the Western blot.
PD-L1-CD80 interactions are required for intracellular signaling necessary for dendritic cell migration.
Sci Adv
January 2025
Department of Medicine, Division of Gastroenterology and Hepatology, University of Colorado School of Medicine, Aurora, CO, USA.
Programmed cell death protein 1 (PD-1) and programmed death ligand 1 (PD-L1) interactions are targets for immunotherapies aimed to reinvigorate T cell function. Recently, it was documented that PD-L1 regulates dendritic cell (DC) migration through intracellular signaling events. In this study, we find that both preclinical murine and clinically available human PD-L1 antibodies limit DC migration.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!