scholarly journals Effect of 17 β‐estradiol on the intracellular calcium concentration and eNOS protein expression in human endothelial cells

2006 ◽  
Vol 20 (4) ◽  
Author(s):  
Der Thor ◽  
Aditya Goel ◽  
Roshanak Rahimian
Keyword(s):  
Endothelial Cells ◽  
Protein Expression ◽  
Intracellular Calcium ◽  
Calcium Concentration ◽  
Intracellular Calcium Concentration ◽  
Human Endothelial Cells ◽  
Enos Protein Expression ◽  
Enos Protein

Effect of hypoxia upon intracellular calcium concentration of human endothelial cells

1992 ◽  
Vol 152 (1) ◽  
pp. 215-221 ◽  
Author(s):  
Thierry Arnould ◽  
Carine Michiels ◽  
Isabelle Alexandre ◽  
Jos� Remacle
Keyword(s):  
Endothelial Cells ◽  
Intracellular Calcium ◽  
Calcium Concentration ◽  
Intracellular Calcium Concentration ◽  
Human Endothelial Cells

Heterogeneous response of microvascular endothelial cells to shear stress

2006 ◽  
Vol 290 (6) ◽  
pp. H2498-H2508 ◽  
Author(s):  
D. Hong ◽  
D. Jaron ◽  
D. G. Buerk ◽  
K. A. Barbee
Keyword(s):  
Endothelial Cells ◽  
Shear Stress ◽  
Intracellular Calcium ◽  
Purinergic Receptors ◽  
Calcium Concentration ◽  
Intracellular Calcium Concentration ◽  
Calcium Signal ◽  
Calcium Waves ◽  
Aortic Endothelial Cells ◽  
Atp Concentration

We investigated changes in calcium concentration in cultured bovine aortic endothelial cells (BAECs) and rat adrenomedulary endothelial cells (RAMECs, microvascular) in response to different levels of shear stress. In BAECs, the onset of shear stress elicited a transient increase in intracellular calcium concentration that was spatially uniform, synchronous, and dose dependent. In contrast, the response of RAMECs was heterogeneous in time and space. Shear stress induced calcium waves that originated from one or several cells and propagated to neighboring cells. The number and size of the responding groups of cells did not depend on the magnitude of shear stress or the magnitude of the calcium change in the responding cells. The initiation and the propagation of calcium waves in RAMECs were significantly suppressed under conditions in which either purinergic receptors were blocked by suramin or extracellular ATP was degraded by apyrase. Exogenously applied ATP produced similarly heterogeneous responses. The number of responding cells was dependent on ATP concentration, but the magnitude of the calcium change was not. Our data suggest that shear stress stimulates RAMECs to release ATP, causing the increase in intracellular calcium concentration via purinergic receptors in cells that are heterogeneously sensitive to ATP. The propagation of the calcium signal is also mediated by ATP, and the spatial pattern suggests a locally elevated ATP concentration in the vicinity of the initially responding cells.

scholarly journals The effect of the calcium-antagonist nitrendipine on intracellular calcium concentration in endothelial cells

1996 ◽  
Vol 118 (8) ◽  
pp. 1899-1904 ◽  
Author(s):  
Aida Salameh ◽  
Gunhild Schomecker ◽  
Katja Breitkopf ◽  
Stefan Dhein ◽  
Wolfgang Klaus
Keyword(s):  
Endothelial Cells ◽  
Calcium Antagonist ◽  
Intracellular Calcium ◽  
Calcium Concentration ◽  
Intracellular Calcium Concentration

scholarly journals Activation of the Mitogen-Activated Protein Kinase Cascade Is Necessary But Not Sufficient for Basic Fibroblast Growth Factor- and Epidermal Growth Factor-Stimulated Expression of Endothelial Nitric Oxide Synthase in Ovine Fetoplacental Artery Endothelial Cells*

Endocrinology ◽  
1999 ◽  
Vol 140 (3) ◽  
pp. 1399-1407 ◽  
Author(s):  
Jing Zheng ◽  
Ian M. Bird ◽  
Amy N. Melsaether ◽  
Ronald R. Magness
Keyword(s):  
Nitric Oxide ◽  
Endothelial Cells ◽  
Growth Factors ◽  
Growth Factor ◽  
Protein Expression ◽  
Mapk Cascade ◽  
Mitogen Activated Protein Kinase ◽  
Mitogen Activated Protein ◽  
Enos Protein Expression ◽  
Enos Protein

Abstract Basic fibroblast growth factor (bFGF), epidermal growth factor (EGF), and vascular endothelial growth factor (VEGF) may play important roles in the placental vasculature, not only by controlling cell growth and differentiation, but also by mediating production of local vasodilators such as nitric oxide. As the mitogen-activated protein kinase (MAPK) signal cascade has been widely associated with cell growth in response to growth factors, herein we investigate whether bFGF, EGF, and VEGF also stimulate expression of endothelial nitric oxide synthase (eNOS) via activation of the MAPK cascade in ovine fetoplacental artery endothelial cells. The presence of the receptors for all three growth factors was confirmed by both immunocytochemistry and a functional cell proliferation assay. All three growth factors at 10 ng/ml rapidly (<10 min) activated MAPK. This activation was inhibited by PD 98059, a specific MAPK kinase inhibitor. bFGF and EGF, but not VEGF, dose- and time-dependently increased eNOS protein levels. Maximal stimulatory effects of bFGF and EGF on eNOS protein expression were observed at 10 ng/ml for 24 h of treatment and were associated with elevated eNOS messenger RNA. PD 98059 also significantly inhibited bFGF- and EGF-induced increases in eNOS protein expression. Because treatment with all three growth factors resulted in activation of the MAPK cascade, while bFGF and EGF, but not VEGF, increased eNOS expression, we conclude that activation of the MAPK cascade is necessary, but not sufficient, for bFGF- and EGF-induced increases in eNOS protein expression in ovine fetoplacental artery endothelial cells. Thus, additional signaling pathways are implicated in the different controls of eNOS expression and mitogenesis by growth factors.

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