Aliskiren attenuates the effects of interleukin-6 on endothelial nitric oxide synthase and caveolin-1 in human aortic endothelial cells

Nitric Oxide ◽  
2016 ◽  
Vol 61 ◽  
pp. 45-54 ◽  
Author(s):  
Ming-Jui Hung ◽  
Yu-Cheng Kao ◽  
Chun-Tai Mao ◽  
Tien-Hsin Chen ◽  
Wei-Siang Chen
Keyword(s):  
Nitric Oxide ◽  
Endothelial Cells ◽  
Nitric Oxide Synthase ◽  
Interleukin 6 ◽  
Endothelial Nitric Oxide Synthase ◽  
Aortic Endothelial Cells ◽  
Caveolin 1 ◽  
Oxide Synthase ◽  
Endothelial Nitric Oxide ◽  
Human Aortic Endothelial Cells

scholarly journals GABABReceptors Expressed in Human Aortic Endothelial Cells Mediate Intracellular Calcium Concentration Regulation and Endothelial Nitric Oxide Synthase Translocation

2014 ◽  
Vol 2014 ◽  
pp. 1-8 ◽  
Author(s):  
Xu-Ping Wang ◽  
Zhen-Ying Cheng ◽  
Katrina L. Schmid
Keyword(s):  
Nitric Oxide ◽  
Endothelial Cells ◽  
Nitric Oxide Synthase ◽  
Endothelial Nitric Oxide Synthase ◽  
Receptor Activation ◽  
Aortic Endothelial Cells ◽  
Oxide Synthase ◽  
Endothelial Nitric Oxide ◽  
Human Aortic Endothelial Cells ◽  
Aortic Endothelial

GABABreceptors regulate the intracellular Ca2+concentration ([Ca2+]i) in a number of cells (e.g., retina, airway epithelium and smooth muscle), but whether they are expressed in vascular endothelial cells and similarly regulate the [Ca2+]iis not known. The purpose of this study was to investigate the expression of GABABreceptors, a subclass of receptors to the inhibitory neurotransmitterγ-aminobutyric acid (GABA), in cultured human aortic endothelial cells (HAECs), and to explore if altering receptor activation modified [Ca2+]iand endothelial nitric oxide synthase (eNOS) translocation. Real-time PCR, western blots and immunofluorescence were used to determine the expression of GABAB1and GABAB2in cultured HAECs. The effects of GABABreceptors on [Ca2+]iin cultured HAECs were demonstrated using fluo-3. The influence of GABABreceptors on eNOS translocation was assessed by immunocytochemistry. Both GABAB1and GABAB2mRNA and protein were expressed in cultured HAECs, and the GABAB1and GABAB2proteins were colocated in the cell membrane and cytoplasm. One hundredμM baclofen caused a transient increase of [Ca2+]iand eNOS translocation in cultured HAECs, and the effects were attenuated by pretreatment with the selective GABABreceptor antagonists CGP46381 and CGP55845. GABABreceptors are expressed in HAECs and regulate the [Ca2+]iand eNOS translocation. Cultures of HAECs may be a usefulin vitromodel for the study of GABABreceptors and vascular biology.

scholarly journals Phytoestrogen Genistein Up-Regulates Endothelial Nitric Oxide Synthase Expression Via Activation of cAMP Response Element-Binding Protein in Human Aortic Endothelial Cells

Endocrinology ◽  
2012 ◽  
Vol 153 (7) ◽  
pp. 3190-3198 ◽  
Author(s):  
Hongwei Si ◽  
Jie Yu ◽  
Hongling Jiang ◽  
Hazel Lum ◽  
Dongmin Liu
Keyword(s):  
Nitric Oxide ◽  
Endothelial Cells ◽  
Endothelial Nitric Oxide Synthase ◽  
No Production ◽  
Enos Expression ◽  
Camp Response Element ◽  
Aortic Endothelial Cells ◽  
Oxide Synthase ◽  
Endothelial Nitric Oxide ◽  
Human Aortic Endothelial Cells

We previously reported that genistein, a phytoestrogen, up-regulates endothelial nitric oxide synthase (eNOS) and prevents hypertension in rats that are independent of estrogen signaling machinery. However, how genistein regulates eNOS expression is unknown. In the present study, we show that genistein enhanced eNOS expression and NO synthesis in primary human aortic endothelial cells. Inhibition of extracellular signal regulated kinase, phosphoinositol-3 kinase, or protein kinase C did not affect genistein-enhanced eNOS expression and NO synthesis. However, chemical inhibition of protein kinase A (PKA) or adenoviral transfer of the specific endogenous PKA inhibitor gene completely abolished PKA activity and genistein-stimulated eNOS expression and NO production. Accordingly, genistein induced PKA activity and subsequent phosphorylation of cAMP response element (CRE)-binding protein (CREB) at Ser133. Suppression of CREB by small interfering RNA transfection abolished genistein-enhanced eNOS expression and NO production. Consistently, deletion of the CRE site within human eNOS promoter eliminated genistein-stimulated eNOS promoter activity. These findings provide the first evidence to our knowledge that genistein may play a beneficial role in vascular function through targeting the PKA/CREB/eNOS/NO signaling pathway.

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