Retinoic acid suppression of endothelial nitric oxide synthase in porcine oocyte

2002 ◽  
Vol 80 (8) ◽  
pp. 777-782 ◽  
Author(s):  
Masa-aki Hattori ◽  
Yukio Kato ◽  
Noboru Fujihara
Keyword(s):  
Nitric Oxide ◽  
Retinoic Acid ◽  
Nitric Oxide Synthase ◽  
Endothelial Nitric Oxide Synthase ◽  
Mrna Level ◽  
Dependent Manner ◽  
Hormonal Stimulation ◽  
Enos Mrna ◽  
Oxide Synthase ◽  
Endothelial Nitric Oxide

The presence of endothelial nitric oxide synthase (eNOS) has been found in porcine oocytes, but its mRNA and protein levels remain relatively constant during hormonal stimulation. The present study was designed to determine the effect of retinoic acid on eNOS regulation in porcine oocytes during follicle-stimulating hormone (FSH) stimulation. Cumulus–oocyte complexes (COCs), prepared from small antral follicles of immature porcine ovaries, were cultured for 15 h and treated with FSH for an additional 48 h. eNOS mRNA and its protein were analyzed by reverse transcription – polymerase chain reaction and Western blotting, respectively. Retinoic acid had an inhibitory effect on the level of oocyte eNOS mRNA in a dose-dependent manner if COCs were exposed to retinoic acid before FSH stimulation. The inhibition of FSH action was reflected in a decrease in expression of c-fos mRNA. eNOS protein also decreased to approximately 50% of the control after exposure to 10 μM retinoic acid. However, the ability of NO synthesis was abolished in the oocytes prepared from retinoic acid pretreated COCs. These results suggest that retinoic acid has a strong inhibitory action on eNOS mRNA level and NO synthesis in the porcine oocyte.Key words: oocyte, retinoic acid, NO synthesis, eNOS, RT–PCR.

Expression of endothelial nitric oxide synthase in the postnatal developing porcine kidney

2001 ◽  
Vol 280 (5) ◽  
pp. R1269-R1275 ◽  
Author(s):  
Michael J. Solhaug ◽  
Usa Kullaprawithaya ◽  
Xui Q. Dong ◽  
Ke-Wen Dong
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Protein Content ◽  
Endothelial Nitric Oxide Synthase ◽  
Enos Expression ◽  
Developmentally Regulated ◽  
Enos Mrna ◽  
Oxide Synthase ◽  
Endothelial Nitric Oxide ◽  
Enos Protein

The postnatal pattern of renal endothelial nitric oxide synthase (eNOS) is unknown. The purpose of this study was to characterize eNOS expression during maturation and compare this to neuronal NOS (nNOS). The experiments measured whole kidney eNOS mRNA expression by RT-PCR and protein content by Western blot, as well as cortical and medullary protein content in piglets at selected postnatal ages and in adult pigs. Whole kidney eNOS mRNA was compared with nNOS. Whole kidney eNOS expression decreased from the newborn to its lowest at 7 days, returning by 14 days to adult levels. This eNOS mRNA pattern contrasted with nNOS, which was highest at birth, and progressively decreased to its lowest level in the adult. At birth, cortical eNOS protein was greater than medullary, contrasting with the adult pattern of equivalent levels. In conclusion eNOS is developmentally regulated during early renal maturation and may critically participate in renal function during this period. The eNOS developmental pattern differs from nNOS, suggesting that these isoforms may have different regulatory factors and functional contributions in the postnatal kidney.

scholarly journals Endothelial nitric oxide synthase activation is required for heparin receptor effects on vascular smooth muscle cells

2020 ◽  
Vol 318 (3) ◽  
pp. C463-C475
Author(s):  
Yaqiu Li ◽  
Leanna M. Talotta-Altenburg ◽  
Kayli A. Silimperi ◽  
Grace O. Ciabattoni ◽  
Linda J. Lowe-Krentz
Keyword(s):  
Nitric Oxide ◽  
Endothelial Cells ◽  
Smooth Muscle ◽  
Nitric Oxide Synthase ◽  
Vascular Smooth Muscle ◽  
Endothelial Nitric Oxide Synthase ◽  
Dependent Manner ◽  
Heparin Treatment ◽  
Oxide Synthase ◽  
Endothelial Nitric Oxide

Published studies indicate that TMEM184A is a heparin receptor that interacts with and transduces stimulation from heparin in vascular cells. Previous studies have indicated that heparin increases endothelial nitric oxide synthase (eNOS) activity in bovine endothelial cells. However, the precise mechanism remains unknown. In this study, we investigated the impact of heparin treatment and TMEM184A on eNOS’s activation and the role of eNOS in heparin signaling in the cloned A7r5 rat vascular smooth muscle cell line and confirmed results in endothelial cells. We employed a combination of TMEM184A knockdown A7r5 cells along with transient eNOS knockdown and enzyme inhibitor strategies. The results indicate that heparin induces phosphorylation of eNOS. eNOS can be immunoprecipitated with TMEM184A and is internalized to the perinuclear region in a TMEM184A-dependent manner in response to heparin. We also examined how heparin treatment leads to phosphorylation of eNOS and confirmed that TMEM184A and Ca2+ were required to mediate heparin-elicited eNOS phosphorylation. Evidence supporting the involvement of transient receptor potential cation channel subfamily V member 4 with TMEM184A in this eNOS activation process is also presented.

scholarly journals Progesterone promotes endothelial nitric oxide synthase expression through enhancing nuclear progesterone receptor-SP-1 formation

2020 ◽  
Vol 319 (2) ◽  
pp. H341-H348
Author(s):  
Yuehua You ◽  
Wanying Tan ◽  
Yongzheng Guo ◽  
Minghao Luo ◽  
Fei-fei Shang ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Progesterone Receptor ◽  
Endothelial Nitric Oxide Synthase ◽  
Dependent Manner ◽  
Enos Expression ◽  
Specificity Protein 1 ◽  
Specificity Protein ◽  
Oxide Synthase ◽  
Endothelial Nitric Oxide

Progesterone directly upregulated endothelial nitric oxide synthase (eNOS) expression in human endothelial cells. Progesterone augmented eNOS promoter activity through a progesterone receptor A- and specificity protein-1-dependent manner. Antagonism of the progesterone receptor reduced eNOS expression and impaired vasodilation in rats.

Lack of endothelial nitric oxide synthase decreases cardiomyocyte proliferation and delays cardiac maturation

2006 ◽  
Vol 291 (6) ◽  
pp. C1240-C1246 ◽  
Author(s):  
Erin Lepic ◽  
Dylan Burger ◽  
Xiangru Lu ◽  
Wei Song ◽  
Qingping Feng
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Endothelial Nitric Oxide Synthase ◽  
Brdu Incorporation ◽  
No Production ◽  
Dependent Manner ◽  
Cardiomyocyte Proliferation ◽  
Cell Counts ◽  
Oxide Synthase ◽  
Endothelial Nitric Oxide

We recently demonstrated that deficiency in endothelial nitric oxide synthase (eNOS) results in congenital septal defects and postnatal heart failure. The aim of this study was to investigate the role of eNOS in cardiomyocyte proliferation and maturation during postnatal development. Cultured eNOS knockout (eNOS−/−) cardiomyocytes displayed fewer cells and lower bromodeoxyuridine (BrdU) incorporation in vitro compared with wild-type (WT) cardiomyocytes ( P < 0.05). Treatment with the nitric oxide (NO) donor diethylenetriamine NONOate increased BrdU incorporation and cell counts in eNOS−/− cardiomyocytes ( P < 0.05). Inhibition of nitric oxide synthase activity using NG-nitro-l-arginine methyl ester decreased the level of BrdU incorporation and cell counts in WT cardiomyocytes ( P < 0.05). Vascular endothelial growth factor (VEGF) increased the level of BrdU incorporation in cultured WT cardiomyocytes in a dose- and time-dependent manner ( P < 0.05). Conversely, VEGF did not alter BrdU incorporation in eNOS−/− cardiomyocytes ( P = not significant). Furthermore, deficiency in eNOS significantly decreased BrdU labeling indexes in neonatal hearts in vivo. Although WT hearts displayed a rapid decrease in atrial natriuretic peptide (ANP) expression in the first week of neonatal life, ANP expression in eNOS−/− hearts remain elevated. Our study demonstrated that NO production from eNOS is necessary for postnatal cardiomyocyte proliferation and maturation, suggesting that eNOS plays an important role during postnatal heart development.

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