ArticleMedical science monitor : international medical journal of experimental and clinical research2017
Regulation of c-Jun N-Terminal Protein Kinase (JNK) Pathway in Apoptosis of Endothelial Outgrowth Cells Induced by Asymmetric Dimethylarginine.
Article in Medical science monitor : international medical journal of experimental and clinical research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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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.
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Who cites it
3 citing papers in PubMed, 3 citations in OpenAlex.
- Role of Endothelial Progenitor Cells in Frailty.International journal of molecular sciences · 2023Review
- DDAH1 Protects against Acetaminophen-Induced Liver Hepatoxicity in Mice.Antioxidants (Basel, Switzerland) · 2022Article
- Overexpression of miR-26b decreases the cisplatin-resistance in laryngeal cancer by targeting ATF2.Oncotarget · 2017Article
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BACKGROUND Endothelial outgrowth cells (EOCs) are terminal endothelial progenitor cells (EPCs). Asymmetric dimethylarginine (ADMA) has been identified as a novel risk factor for cardiovascular diseases. Our aim in the present study was to investigate the effect of regulation of asymmetric dimethylarginine (ADMA) on EOCs apoptosis and to explore the underlining mechanisms of c-Jun N-terminal protein kinase (JNK) pathway in the process. MATERIAL AND METHODS EOCs were harvested from umbilical cord blood and obtained by using density gradient centrifugation and adhesive culture methods. Endothelial characteristics were identified by immunohistochemistry and fluorescence staining. EOCs were treated with different concentrations of ADMA and detected by flow cytometry. After JNK specific inhibitor (SP600125) was added, EOCs apoptosis protein expressions were measured by Western blot analysis. Proliferation, migration, and vascularization were detected by CCK-8 assay, wound healing assay, and tube-like formation assay, respectively. RESULTS EOCs were successfully extracted from umbilical cord blood and different concentrations of ADMA aggravated EOCs apoptosis. ADMA distinctly activates the phosphorylation activity of JNK. Supplementation of JNK-specific inhibitor (SP600125) decreased expression of Bax and cleaved caspase 3/9, and alleviated ADMA-induced apoptosis. SP600125 also promoted angiogenesis viability. CONCLUSIONS The JNK pathway participates in the apoptosis-promoting process of EOCs, and targeted inhibition of the JNK pathway can alleviate ADMA-induced injury, which I s the potential underlying mechanism of vascular endothelium injury in ischemic stroke.
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