ArticleAmerican journal of translational research2019
Antagonism of P2Y11 receptor (P2Y11R) protects epidermal stem cells against UV-B irradiation.
Article in American journal of translational research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
4 citing papers in PubMed, 7 citations in OpenAlex.
- Shigella infection is facilitated by interaction of human enteric α-defensin 5 with colonic epithelial receptor P2Y11.Nature microbiology · 2025Article
- Annexin A1 protects epidermal stem cells against ultraviolet-B irradiation-induced mitochondrial dysfunction.Archives of dermatological research · 2024Article
- Influence of chlorpyrifos exposure on UVB irradiation induced toxicity in human skin cells.Journal of occupational medicine and toxicology (London, England) · 2023Article
- Differential Expression Profiles and Function Predictions for tRFs & tiRNAs in Skin Injury Induced by Ultraviolet Irradiation.Frontiers in cell and developmental biology · 2021Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Epidermal stem cells (ESCs) play essential roles in maintaining skin homeostasis and cell turnover of skin. Long-term exposure to UV-B irradiation induces a decrease in the population of ESCs and impairs the capacities of ESCs. The P2Y11 receptor (P2Y11R) is an important member of the P2 receptor family and plays a key role in mediating purinergic signaling and intracellular effects. In this study, we found that UV-B irradiation induced an increase in P2Y11R in ESCs. Antagonism of P2Y11R using NF157 ameliorated UV-B irradiation-induced oxidative stress by reducing reactive oxygen species (ROS) production and NADPH oxidase-4 (NOX-4) expression. Additionally, treatment with NF157 had a protective effect against UV-B irradiation-induced mitochondrial dysfunction by increasing mitochondrial membrane potential (MMP) and cytochrome c oxidase activity. Also, NF157 could mitigate lactate dehydrogenase (LDH) release and decreased the tumor necrosis factor-↑ (TNF-α), interleukin-6 (IL-6), and IL-8 secretion. Importantly, we found that treatment with NF157 attenuated UV-B irradiation-induced loss of ESCs capability by restoring the expression of integrin β1 and Krt19. Mechanistically, treatment with NF157 prevented UV-B irradiation-induced destruction of the Wnt/β-catenin signaling transduction pathway by increasing the expression of Wnt1, Wnt3a, c-Myc, and cyclin D1. These findings suggest a novel function of P2Y11R in regulating the capacities of ESCs upon UV-B irradiation.
Indexed as
Identifiers
31497195PMC6731446W2996782164What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.