ArticleLupus science & medicine2019
L-sepiapterin restores SLE serum-induced markers of endothelial function in endothelial cells.
Article in Lupus science & medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 13 citations in OpenAlex.
- The endothelium response to kidney injury.Nature reviews. Nephrology · 2026Review
- Article
- Lupus nephritis serum induces changes in gene expression in human glomerular endothelial cells, which is modulated by L-sepiapterin: implications for redox-mediated endothelial dysfunction.Lupus science & medicine · 2025Article
- Reprogramming of breast tumor-associated macrophages with modulation of arginine metabolism.Life science alliance · 2024Article
- Reprogramming of breast tumor-associated macrophages with modulation of arginine metabolism.bioRxiv : the preprint server for biology · 2023Article
- Endothelial cell activation and glycocalyx shedding - potential as biomarkers in patients with lupus nephritis.Frontiers in immunology · 2023Review
- Endothelial cells: potential novel regulators of renal inflammation.American journal of physiology. Renal physiology · 2022Review
- Lupus serum induces inflammatory interaction with neutrophils in human glomerular endothelial cells.Lupus science & medicine · 2020Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
objectiveSLE serves as an independent risk factor` for endothelial dysfunction (ED) not explained by Framingham risk factors. We sought to understand the development of SLE-induced ED on a cellular level in order to develop strategies aimed at reversing cellular abnormalities. This study assessed the impact of SLE patient serum on endothelial nitric oxide synthase (eNOS), nitric oxide (NO) production and functional changes in the cell.
methodsHuman umbilical vein endothelial cells (HUVECs) cultured in serum of either SLE (n=25) or healthy patients (n=14) or endothelial basal medium 2 (EBM-2) culture media supplemented with fetal bovine serum with or without L-sepiapterin were used for our studies. We applied the fluorescent probe DAF-FM diacetate for intracellular NO detection using flow cytometry. Total RNA isolates were analysed using reverse transcription PCR for eNOS mRNA expression. Oxygen consumption rate was determined using seahorse analysis. Neutrophil adhesion and migration were determined using a calcein AM microscopy assay.
resultsThe mRNA expression of eNOS was increased in SLE cultured HUVECs compared with healthy control (p<0.05). The SLE eNOS mRNA level correlated with SLE patient age (p=0.008); however, this trend was not observed with healthy patients. SLE serum reduced NO production in HUVECs compared with EBM-2 cultured cells (p<0.05). Co-treatment of endothelial cells with L-sepiapterin preserved HUVEC capacity to produce NO in SLE conditions (p<0.01). SLE serum enhanced neutrophil migration (p<0.01) but not neutrophil adhesion compared with healthy controls. The bioenergetic health index was not different.
conclusionsSLE likely causes disruption of endothelial cell eNOS function and NO modulated pathways.
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