ArticleIranian journal of basic medical sciences2018
S100A9 aggravates bleomycin-induced dermal fibrosis in mice via activation of ERK1/2 MAPK and NF-κB pathways.
Article in Iranian journal of basic medical sciences, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 8 citations in OpenAlex.
- The RAGE Pathway in Skin Pathology Development: A Comprehensive Review of Its Role and Therapeutic Potential.International journal of molecular sciences · 2024Review
- Characteristics of Interstitial Pneumonia With Autoimmune Features (IPAF): Protocol for a Multicenter Prospective Study.JMIR research protocols · 2023Article
- S100 calcium-binding protein A9 promotes skin regeneration through toll-like receptor 4 during tissue expansion.Burns & trauma · 2023Article
- Yi-Shen-Hua-Shi Granule Alleviates Adriamycin-Induced Glomerular Fibrosis by Suppressing the BMP2/Smad Signaling Pathway.Frontiers in pharmacology · 2022Article
- JUN promotes hypertrophic skin scarring via CD36 in preclinical in vitro and in vivo models.Science translational medicine · 2021Article
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectivesThis study aims to investigate the pathogenicity and possible mechanisms of S100A9 function in mice models of scleroderma. MATERIALS AND
methodsThe content of S100A9 in the skin tissues of mice with scleroderma was determined. Different concentrations of bleomycin (BLM) and S100A9 were subcutaneously injected into the backs of mice simultaneously, and then pathological changes in the skin of these mice were monitored. Specifically, the levels of inflammatory cytokines and alpha smooth muscle actin (α-SMA), the activation of extracellular regulated kinase 1/2 (ERK1/2), mitogen-activated protein kinase (MAPK) and nuclear factor-kappa B (NF-κB) pathways, and the expression of the receptor for advanced glycation end-product (RAGE) in the skin were determined.
resultsThe content of S100A9 in the skin tissues of mice with scleroderma was determined. Different concentrations of BLM and S100A9 were subcutaneously injected into the backs of mice simultaneously, and then pathological changes in the skin of these mice were monitored. Specifically, the levels of inflammatory cytokines and alpha smooth muscle actin (α-SMA), the activation of extracellular regulated kinase 1/2 (ERK1/2) mitogen-activated protein kinase (MAPK) and nuclear factor-kappa B (NF-κB) pathways, and the expression of the receptor for advanced glycation end-product (RAGE) in the skin were determined.
conclusionS100A9 aggravates dermal fibrosis in BLM-induced scleroderma (BIS) mice, and its mechanisms might be mediated by RAGE, ERK1/2, and NF-κB pathway.
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Registered trials
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