Thiazolidinediones Suppress Endothelin-1 Secretion from Bovine Vascular Endothelial Cells: A New Possible Role of PPARγ on Vascular Endothelial Function

1999 ◽  
Vol 254 (3) ◽  
pp. 757-763 ◽  
Author(s):  
Hiroaki Satoh ◽  
Kazuhisa Tsukamoto ◽  
Yoshiaki Hashimoto ◽  
Naoaki Hashimoto ◽  
Masako Togo ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Endothelial Function ◽  
Vascular Endothelial Cells ◽  
Vascular Endothelial ◽  
Vascular Endothelial Function ◽  
Endothelin 1

scholarly journals Vascular Endothelial Estrogen Receptor α Is Modulated by Estrogen Status and Related to Endothelial Function and Endothelial Nitric Oxide Synthase in Healthy Women

2009 ◽  
Vol 30 (5) ◽  
pp. 542-542
Author(s):  
Kathleen M. Gavin ◽  
Douglas R. Seals ◽  
Annemarie E. Silver ◽  
Kerrie L. Moreau
Keyword(s):  
Endothelial Cells ◽  
Menstrual Cycle ◽  
Endothelial Function ◽  
Postmenopausal Women ◽  
Vascular Endothelial Cells ◽  
Premenopausal Women ◽  
Estrogen Receptor Α ◽  
Vascular Endothelial ◽  
Vascular Endothelial Function ◽  
Endothelial Nitric Oxide

ABSTRACT Context and Objective Estrogen receptor α (ERα), a potent transcription factor expressed in vascular endothelial cells, plays a key role in regulating vascular function and health. We determined whether vascular endothelial cell expression of ERα is influenced by estrogen status and is related to vascular endothelial function in healthy women. Methods ERα protein expression was measured (quantitative immunofluorescence) in endothelial cells from peripheral veins of 16 healthy, premenopausal women during the early follicular (EF) and late follicular (LF) phases of the menstrual cycle and 17 estrogen-deficient postmenopausal women. Endothelial-dependent dilation (EDD; brachial artery flow-mediated dilation) and endothelial nitric oxide synthase (eNOS) expression and activation were also measured in a subgroup of women. Results In premenopausal women (n = 10), ERα expression was 30% lower (P < 0.001) during the EF (low estrogen) compared with the LF (high estrogen) phase of the menstrual cycle. In postmenopausal women, ERα expression was 33% lower (P < 0.001) compared with the LF phase of the menstrual cycle in premenopausal women. ERα expression was strongly related (r = 0.67; P < 0.001) to EDD, which was reduced in postmenopausal women. ERα abundance was positively related to expression of eNOS (r = 0.54; P = 0.009; n = 21) and ser1177 phosphorylated eNOS (r = 0.59; P = 0.006; n = 20). Conclusions These results provide the first evidence that expression of ERα in vascular endothelial cells is modulated by estrogen status and may be a key determinant of vascular endothelial function in healthy pre- and postmenopausal women. ERα expression may influence vascular endothelial function in women by affecting protein levels and activation of eNOS.

scholarly journals Study on Damage Mechanism and Repair of Vascular Endothelial Cells Based on Ultrasound Technology

2021 ◽  
Vol 2021 ◽  
pp. 1-9
Author(s):  
Shuhao Deng ◽  
Quan Jiang ◽  
Xin Lu ◽  
Yuan Zhang
Keyword(s):  
Endothelial Cells ◽  
Endothelial Function ◽  
Relaxation Function ◽  
Vascular Endothelial Cells ◽  
Early Stage ◽  
Gradient Centrifugation ◽  
Control Group ◽  
Dependent Manner ◽  
Vascular Endothelial ◽  
Vascular Endothelial Function

Objective. To detect the endothelial function of external iliac artery in rats with different stages of atherosclerosis by high-resolution ultrasound, so as to provide experimental methodological basis for evaluating the function of vascular endothelial cells by ultrasound. Methods. The animals were randomly divided into the control group ( n = 6 ) and the atherosclerosis model group ( n = 15 ). The atherosclerosis group was further divided into 4-week group, 8-week group, and 12-week group, with 5 animals in each group. After separating and grinding rat spleen, the obtained cells were cultured by density gradient centrifugation. After the cells adhered, the morphology of the cells was observed under a microscope and identified by DiI-Ac-LDL and FITC-UEA-I double staining. The activities of LDH and SOD, the contents of MDA and GSH, and the contents of NO in plasma were detected by biochemical methods. Results. The protective effect of rosanilin on brain injury in rats with acute hypobaric hypoxia and its regulation on the expression of pAkt protein; ox-LDL inhibited the proliferation activity of EPCs in a concentration-dependent manner. The expression of KLF2 and S1PR1 in HAEC can be knocked down by small interfering RNA, and knocking down KLF2 can not only downregulate the expression of S1PR1 but also downregulate HAVEN. With the development of atherosclerosis, the endothelium-dependent relaxation function and endothelium-independent relaxation function of the control group and the atherosclerosis model at 4, 8, and 12 weeks were damaged in different degrees and gradually aggravated. Conclusion. Atherosclerosis is a disease with both morphological and functional damage, and vascular endothelial function is damaged in the early stage with corresponding pathological changes. Ultrasound is an effective method to evaluate vascular endothelial function.

scholarly journals Role of endothelin-1 and its receptors, ETAand ETB, in the survival of human vascular endothelial cells

2017 ◽  
Vol 95 (10) ◽  
pp. 1298-1305 ◽  
Author(s):  
Marianne Mikhail ◽  
Pierre H. Vachon ◽  
Pedro D’Orléans-Juste ◽  
Danielle Jacques ◽  
Ghassan Bkaily
Keyword(s):  
Endothelial Cells ◽  
Caspase 3 ◽  
Vascular Endothelial Cells ◽  
Vascular Endothelial ◽  
Endothelin 1 ◽  
Apoptotic Effect

Our previous work showed the presence of endothelin-1 (ET-1) receptors, ETAand ETB, in human vascular endothelial cells (hVECs). In this study, we wanted to verify whether ET-1 plays a role in the survival of hVECs via the activation of its receptors ETAand (or) ETB(ETAR and ETBR, respectively). Our results showed that treatment of hVECs with ET-1 prevented apoptosis induced by genistein, an effect that was mimicked by treatment with ETBR-specific agonist IRL1620. Furthermore, blockade of ETBR with the selective ETBR antagonist A-192621 prevented the anti-apoptotic effect of ET-1 in hVECs. However, activation of ETAreceptor alone did not seem to contribute to the anti-apoptotic effect of ET-1. In addition, the anti-apoptotic effect of ETBR was found to be associated with caspase 3 inhibition and does not depend on the density of this type of receptor. In conclusion, our results showed that ET-1 possesses an anti-apoptotic effect in hVECs and that this effect is mediated, to a great extent, via the activation of ETBR. This study revealed a new role for ETBR in the survival of hVECs.

scholarly journals Role of the 3′-Untranslated Region of Human Endothelin-1 in Vascular Endothelial Cells

2003 ◽  
Vol 279 (10) ◽  
pp. 8655-8667 ◽  
Author(s):  
Imtiaz A. Mawji ◽  
G. Brett Robb ◽  
Sharon C. Tai ◽  
Philip A. Marsden
Keyword(s):  
Endothelial Cells ◽  
Untranslated Region ◽  
Vascular Endothelial Cells ◽  
Vascular Endothelial ◽  
Endothelin 1

scholarly journals Emerging Role of AP-1 Transcription Factor JunB in Angiogenesis and Vascular Development

2021 ◽  
Vol 22 (6) ◽  
pp. 2804
Author(s):  
Yasuo Yoshitomi ◽  
Takayuki Ikeda ◽  
Hidehito Saito-Takatsuji ◽  
Hideto Yonekura
Keyword(s):  
Endothelial Cells ◽  
Transcription Factor ◽  
Blood Vessel ◽  
Vascular Endothelial Cells ◽  
Vascular Development ◽  
Endothelial Cell Migration ◽  
Vascular Endothelial ◽  
Blood Vessel Formation ◽  
Vessel Formation

Blood vessels are essential for the formation and maintenance of almost all functional tissues. They play fundamental roles in the supply of oxygen and nutrition, as well as development and morphogenesis. Vascular endothelial cells are the main factor in blood vessel formation. Recently, research findings showed heterogeneity in vascular endothelial cells in different tissue/organs. Endothelial cells alter their gene expressions depending on their cell fate or angiogenic states of vascular development in normal and pathological processes. Studies on gene regulation in endothelial cells demonstrated that the activator protein 1 (AP-1) transcription factors are implicated in angiogenesis and vascular development. In particular, it has been revealed that JunB (a member of the AP-1 transcription factor family) is transiently induced in endothelial cells at the angiogenic frontier and controls them on tip cells specification during vascular development. Moreover, JunB plays a role in tissue-specific vascular maturation processes during neurovascular interaction in mouse embryonic skin and retina vasculatures. Thus, JunB appears to be a new angiogenic factor that induces endothelial cell migration and sprouting particularly in neurovascular interaction during vascular development. In this review, we discuss the recently identified role of JunB in endothelial cells and blood vessel formation.

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