ArticleAmerican journal of translational research2017
FGF21 inhibitor suppresses the proliferation and migration of human umbilical vein endothelial cells through the eNOS/PI3K/AKT pathway.
Article in American journal of translational research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 22 citations in OpenAlex.
- The role of nonmyocardial cells in the development of diabetic cardiomyopathy and the protective effects of FGF21: a current understanding.Cell communication and signaling : CCS · 2024Review
- Article
- Fibroblast growth factor 21 in metabolic syndrome.Frontiers in endocrinology · 2023Review
- Fibroblast growth factor 21 resistance is associated with body shape in patients with type 2 diabetes complicating hypertension.Frontiers in cardiovascular medicine · 2023Article
- Fibroblast growth factor 21 reverses high-fat diet-induced impairment of vascular function via the anti-oxidative pathway in ApoE knockout mice.Journal of cellular and molecular medicine · 2022Article
- The Association Between FGF21 and Diabetic Erectile Dysfunction: Evidence from Clinical and Animal Studies.Frontiers in endocrinology · 2022Article
- Long Noncoding RNABioMed research international · 2020Article
- Increased levels of circulating fibroblast growth factor 21 in children with Kawasaki disease.Clinical and experimental medicine · 2019Article
- Enhanced Homing of Mesenchymal Stem Cells Overexpressing Fibroblast Growth Factor 21 to Injury Site in a Mouse Model of Traumatic Brain Injury.International journal of molecular sciences · 2019Article
- Self-Healing and Injectable Hydrogel for Matching Skin Flap Regeneration.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2019Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In this study, we investigated molecular mechanism underlying the regulation of endothelial nitric oxide synthase (eNOS) expression by fibroblast growth factor 21 (FGF21). We analyzed FGF21 and eNOS expression in hypertensive and healthy (control) subjects (n=30/group). To evaluate the effects of FGF21 on endothelial cells, we transfected FGF21 mimics or FGF21 inhibitor into human umbilical vein endothelial cells (HUVECs). Cell proliferation was analyzed using the methyl thiazolyl tetrazolium assay, and cell migration and invasion were assessed using Transwell assays. In addition, eNOS, PI3K, and AKT mRNA in the HUVECs were evaluated by quantitative reverse transcription PCR, and p-eNOS, PI3K, and p-AKT were evaluated by Western blotting. Our results showed increased levels of FGF21 mRNA and eNOS mRNA/protein in the blood of hypertensive patients compared with healthy controls. The FGF21 inhibitor inhibited HUVEC growth, migration, and invasion and significantly decreased eNOS, PI3K, and AKT mRNA levels and p-eNOS, PI3K, and p-AKT protein levels in HUVECs. Treatment with VEGF and/or overexpression of eNOS partially restored cell proliferation and p-AKT levels. Taken together, our results indicate that FGF21 regulates eNOS through the PI3K/AKT pathway.
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Identifiers
29312484PMC5752882W2977334302What OpenQuestion holds
Registered trials
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