ArticleMolecular medicine reports2023
S100A1 expression is increased in spinal cord injury and promotes inflammation, oxidative stress and apoptosis of PC12 cells induced by LPS via ERK signaling.
Article in Molecular medicine reports, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 10 citations in OpenAlex.
- Exercise-derived exosomal miR-151-3p: An innovative anti-inflammatory and antioxidant therapeutic for spinal cord injury.Bioactive materials · 2026Article
- S100A1 Promotes MDM2-Mediated KLF15 Ubiquitination to Regulate ID1-Driven Tubular Injury in Diabetic Kidney Disease.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Article
- Imidazopyridine derivatives as promising anti-RSC advances · 2026Article
- Research article proteomics-based plasma biomarkers for predicting CRKP infection in ICU sepsis patients.Frontiers in pharmacology · 2026Article
- Decoding Preeclampsia and Obesity: The Role of Immune Responses and Natural Product Interventions.Endocrine, metabolic & immune disorders drug targets · 2026Article
- Targeting S100A8/A9: a molecular gateway to oral inflammation, microglial activation and neuroinflammation.Frontiers in immunology · 2026Review
- CuO-NPs Induce Apoptosis and Functional Impairment in BV2 Cells Through the CSF-1R/PLCγ2/ERK/Nrf2 Pathway.Toxics · 2025Article
- The emerging role of cuproptosis in spinal cord injury.Frontiers in immunology · 2025Review
- Regulatory effect of inflammatory mediators in spinal cord injury.Frontiers in immunology · 2025Review
- Investigation of LncRNA Expression Profiles and Analysis of Immune-Related lncRNA-miRNA-mRNA Networks in Neovascular Age-Related Macular Degeneration.Combinatorial chemistry & high throughput screening · 2025Article
- MiR-10b-5p attenuates spinal cord injury and alleviates LPS-induced PC12 cells injury by inhibiting TGF-β1 decay and activating TGF-β1/Smad3 pathway through PTBP1.European journal of medical research · 2024Article
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Spinal cord injury (SCI) is a severe neurological disorder and the molecular mechanisms leading to its poor prognosis remain to be elucidated. S100A1, a mediator of Ca2+ handling of sarcoplasmic reticulum and mitochondrial function, operates as an endogenous danger signal (alarmin) associated with inflammatory response and tissue injury. The aim of the present study was to investigate the expression and biological effects of S100A1 in SCI. A rat model of SCI and a PC12 cell model of lipopolysaccharide (LPS)‑induced inflammation were established to examine S100A1 expression at the mRNA and protein levels. The inflammation level, which was mediated by S100A1, was determined based on inflammatory factor (IL‑1β, IL‑6 and TNF‑α) and anti‑inflammatory factor (IL‑10) expression. The effects of S100A1 on cellular oxidation and anti‑oxidation levels were observed by detecting the levels of reactive oxygen species, superoxide dismutase, catalase activities and nuclear factor erythroid 2‑related factor 2 expression. The protein levels of Bax, Bcl2 and cleaved caspase‑3 were used for the evaluation of the effects of S100A1 on apoptosis. Phosphorylated (p‑)ERK1/2 expression was used to evaluate the effects of S100A1 on ERK signaling. The results revealed that S100A1 expression was significantly upregulated
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