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10.1136/lupus-2018-000294 http://scihub22266oqcxt.onion/10.1136/lupus-2018-000294 31168396!6519412!31168396     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=31168396&cmd=llinks): Failed to open stream: HTTP request failed! HTTP/1.1 429 Too Many Requests in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 215       Lupus+Sci+Med 2019 ; 6 (1): e000294 Nephropedia Template TP {{tp|p=31168396|t=2019. L-sepiapterin restores SLE serum-induced markers of endothelial function in endothelial cells |pdf=|usr=}}{{31168396}} gab.com Text L-sepiapterin restores SLE serum-induced markers of endothelial function in endothelial cells JO: Lupus Sci Med http://www.kidney.de/pget.php?&tw=1&pmid=31168396 #FOAvip OBJECTIVE: SLE 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. METHODS: Human 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. RESULTS: The 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. CONCLUSIONS: SLE likely causes disruption of endothelial cell eNOS function and NO modulated pathways. Twit Text FOAVip L-sepiapterin restores SLE serum-induced markers of endothelial function in endothelial cells ????Lupus Sci Med http://www.kidney.de/pget.php?&tw=1&pmid=31168396 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=31168396 #FOAvip English Wikipedia <ref>{{Cite pmid|31168396}}</ref> L-sepiapterin restores SLE serum-induced markers of endothelial function in endothelial cells #MMPMID31168396 Jones Buie JN; Pleasant Jenkins D; Muise-Helmericks R; Oates JC Lupus Sci Med 2019[]; 6 (1): e000294 PMID31168396show ga OBJECTIVE: SLE 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. METHODS: Human 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. RESULTS: The 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. CONCLUSIONS: SLE likely causes disruption of endothelial cell eNOS function and NO modulated pathways. ?L-sepiapterin restores SLE serum-induced markers of endothelial functi(epmc).pdf DeepDyve Pubget Overpricing