Presence of neuropeptide Y and the Y1 receptor in the plasma membrane and nuclear envelope of human endocardial endothelial cells: modulation of intracellular calcium

2003 ◽  
Vol 81 (3) ◽  
pp. 288-300 ◽  
Author(s):  
Danielle Jacques ◽  
Sawsan Sader ◽  
Claudine Perreault ◽  
Alain Fournier ◽  
Georges Pelletier ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Confocal Microscopy ◽  
Nuclear Envelope ◽  
Neuropeptide Y ◽  
Intracellular Calcium ◽  
Microscopy Technique ◽  
Human Fetal Heart ◽  
Endocardial Endothelial Cells ◽  
Npy Receptors ◽  
Sustained Increase

The aims of the present study were to investigate the presence and distribution of NPY and the Y1 receptor in endocardial endothelial cells (EECs), to verify if EECs can release NPY, and to determine if the effect of NPY on intracellular calcium is mediated via the Y1 receptor. Immunofluorescence, 3-D confocal microscopy and radioimmu noassay techniques were used on 20-week-old human fetal EECs. Our results showed that NPY and the Y1 receptor are present in human EECs (hEECs) and that their distributions are similar, the fluorescence labelling being higher in the nucleus and more particularly at the level of the nuclear envelope when compared with the cytosol. Using radio immunoassay, we demonstrated that EECs are a source of NPY and can secrete this peptide upon a sustained increase of intracellular calcium ([Ca]i). Using fluo-3 and 3-D confocal microscopy technique, superfusion of hEECs as well as EECs isolated from rat adult hearts with increasing concentrations of NPY induced a dose-dependent, sustained increase in free cytosolic and nuclear Ca2+ levels. This effect of NPY on EEC [Ca]i was completely reversible upon washout of NPY and was partially blocked by BIBP3226, a selective Y1 receptor antagonist. The results suggest that NPY and Y1 receptors are present in the EECs of 20-week-old human fetal heart and they share the same distribution and localization inside the cell. In addition, EECs are able to secrete NPY in response to an increase in [Ca]i, and the Y1 receptor as well as other NPY receptors seem to participate in mediating the effects of NPY on [Ca]i in these cells. Thus, NPY released by EECs may modulate excitation–secretion coupling of these cells.Key words: neuropeptide Y (NPY), nuclear envelope receptors, endocardial endothelial cells, NPY receptors, intracellular calcium.

Angiotensin II and its receptors in human endocardial endothelial cells: role in modulating intracellular calcium

2003 ◽  
Vol 81 (3) ◽  
pp. 259-266 ◽  
Author(s):  
Danielle Jacques ◽  
Nelly A. Abdel Malak ◽  
Sawsan Sader ◽  
Claudine Perreault
Keyword(s):  
Endothelial Cells ◽  
Angiotensin Ii ◽  
Confocal Microscopy ◽  
Intracellular Calcium ◽  
Fluorescence Signal ◽  
Ang Ii ◽  
Microscopy Technique ◽  
Endocardial Endothelial Cells ◽  
Microscopy Techniques ◽  
Dose Dependent

he aims of the present study are to investigate the presence and distribution of angiotensin II (Ang II), as well as AT1 and AT2 receptors, in endocardial endothelial cells (EECs) and to determine if the effect of Ang II on intracellular calcium in these cells is mediated via the AT1 or the AT2 receptor. Immunofluorescence and 3D confocal microscopy techniques were used on 20-week-old fetal human EECs. Our results showed that Ang II and its receptors, the AT1 and the AT2 types, are present and exhibit a different distribution in human EECs. Ang II labelling is found throughout the cell with a fluorescence signal higher in the cytosol when compared with the nucleus. Like Ang II, the AT1 receptor fluorescence signal is also homogeneously distributed in human EECs but with a preferential labelling at the level of the nucleus, while the AT2 receptor labelling is solely present in the nucleus. Using fluo-3 and 3D confocal microscopy technique, superfusion of human EECs with increasing concentration of Ang II induced a dose-dependent sustained increase in free cytosolic and nuclear Ca2+ levels. This effect of Ang II on human EEC's intra cellular Ca2+ ([Ca2+]i) was completely prevented by losartan, an AT1 receptor antagonist. Our results suggest that Ang II, as well as AT1 and AT2 receptors, is present but differentially distributed in EECs of 20-week-old fetal human hearts, and that the AT1 receptor mediates the effects of Ang II on [Ca2+]i in these cells.Key words: angiotensin II, nuclear receptors, endocardial endothelial cells, Ang II receptors, intracellular calcium.

Neuropeptide Y and its receptors in ventricular endocardial endothelial cells

2017 ◽  
Vol 95 (10) ◽  
pp. 1224-1229 ◽  
Author(s):  
Danielle Jacques ◽  
Pedro D’Orléans-Juste ◽  
Sheldon Magder ◽  
Ghassan Bkaily
Keyword(s):  
Heart Failure ◽  
Endothelial Cells ◽  
Cardiac Function ◽  
Neuropeptide Y ◽  
Entry And Exit ◽  
Cardiac Pathology ◽  
Contraction Coupling ◽  
Endocardial Endothelial Cells ◽  
The Right ◽  
Cardiac Excitation

Endocardial endothelial cells (EECs) constitute an important component of the heart. These cells form a monolayer that covers the cavities of the right (EECRs) and left (EECLs) ventricles. They play an important role in cardiac excitation–contraction coupling via their secretion of cardioactive factors such as neuropeptide Y (NPY). They also contribute to cardiac pathology such as arrhythmia, hypertrophy, and heart failure. Differences between EECRs and EECLs contribute to tuning of circulating factors at the entry and exit of the ventricles. NPY, via activation of its receptors, modulates the excitation–secretion coupling of EECs, thus, indirectly modulating cardiac function and remodeling.

Differences in neuropeptide Y-induced secretion of endothelin-1 in left and right human endocardial endothelial cells

Neuropeptides ◽  
2012 ◽  
Vol 46 (6) ◽  
pp. 373-382 ◽  
Author(s):  
Dima Abdel-Samad ◽  
Claudine Perreault ◽  
Lena Ahmarani ◽  
Levon Avedanian ◽  
Ghassan Bkaily ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Neuropeptide Y ◽  
Endothelin 1 ◽  
Left And Right ◽  
Endocardial Endothelial Cells

Neuropeptide Y induced increase of cytosolic and nuclear Ca2+ in heart and vascular smooth muscle cells

2000 ◽  
Vol 78 (2) ◽  
pp. 162-172 ◽  
Author(s):  
Danielle Jacques ◽  
Sawsan Sader ◽  
Nesrine El-Bizri ◽  
Sanaa Chouffani ◽  
Ghada Hassan ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Confocal Microscopy ◽  
Vascular Smooth Muscle ◽  
Neuropeptide Y ◽  
Receptor Antagonist ◽  
Spontaneous Contraction ◽  
Receptor Type ◽  
Heart Cells ◽  
Intracellular Ca ◽  
Sustained Increase

It was reported that neuropeptide Y (NPY) affects cardiac and vascular smooth muscle (VSM) function probably by increasing intracellular Ca2+. In this study, using fura-2 microfluorometry and fluo-3 confocal microscopy techniques for intracellular Ca2+ measurement, we attempted to verify whether the action of NPY receptor's stimulation in heart and VSM cells modulates intracellular Ca2+ and whether this effect is mediated via the Y1 receptor type. Using spontaneously contracting single ventricular heart cells of 10-day-old embryonic chicks and the fluo-3 confocal microscopy Ca2+ measurement technique to localize cytosolic ([Ca]c) and nuclear ([Ca]n) free Ca2+ level and distribution, 10-10 M of human (h) NPY significantly (P < 0.05) increased the frequency of cytosolic and nuclear Ca2+ transients during spontaneous contraction. Increasing the concentration of hNPY (10-9 M) did not further increase the frequency of Ca2+ transients. The L-type Ca2+ channel blocker, nifedipine (10-5 M), significantly (P < 0.001) blocked the spontaneous rise of intracellular Ca2+ in the absence and presence of hNPY (10-10 and 10-9 M). However, the selective Y1 receptor antagonist, BIBP3226 (10-6 M), significantly decreased the hNPY-induced (10-10 and 10-9 M) increase in the frequency of Ca2+ transients back to near the control level (P < 0.05). In resting nonworking heart and human aortic VSM cells, hNPY induced a dose-dependent sustained increase of basal resting intracellular Ca2+ with an EC50 near 10-9 M. This sustained increase was cytosolic and nuclear and was completely blocked by the Ca2+ chelator EGTA, and was significantly decreased by the Y1 receptor antagonist BIBP3226 in both heart (P < 0.05) and VSM (P < 0.01) cells. These results strongly suggest that NPY stimulates the resting basal steady-state Ca2+ influx through the sarcolemma and induces sustained increases of cytosolic and nuclear calcium, in good part, via the activation of the sarcolemma membrane Y1 receptor type in both resting heart and VSM cells. In addition, NPY also increased the frequency of Ca2+ transients during spontaneous contraction of heart cells mainly via the activation of the Y1 receptor type, which may explain in part the active cardiovascular action of this peptide.Key words: heart, vascular smooth muscle, neuropeptide Y, BIBP3226, calcium, nucleus.

Ultra-Rapid Freezing of Isolated Skeletal Muscle Fibers

1977 ◽  
Vol 35 ◽  
pp. 576-577
Author(s):  
Joachim R. Sommer ◽  
Nancy R. Wallace
Keyword(s):  
Skeletal Muscle ◽  
Sarcoplasmic Reticulum ◽  
Granular Material ◽  
Nuclear Envelope ◽  
Intracellular Calcium ◽  
Ruthenium Red ◽  
Threshold Concentration ◽  
Rapid Freezing ◽  
Frog Skeletal Muscle ◽  
Electrical Isolation

After Howell (1) had shown that ruthenium red treatment of fixed frog skeletal muscle caused collapse of the intermediate cisternae of the sarcoplasmic reticulum (SR), forming a pentalaminate structure by obi iterating the SR lumen, we demonstrated that the phenomenon involves the entire SR including the nuclear envelope and that it also occurs after treatment with other cations, including calcium (2,3,4).From these observations we have formulated a hypothesis which states that intracellular calcium taken up by the SR at the end of contraction causes the M rete to collapse at a certain threshold concentration as the first step in a subsequent centrifugal zippering of the free SR toward the junctional SR (JSR). This would cause a) bulk transport of SR contents, such as calcium and granular material (4) into the JSR and, b) electrical isolation of the free SR from the JSR.

scholarly journals Sustained increase in intracellular calcium promotes neuronal survival

1991 ◽  
Vol 11 (8) ◽  
pp. 2582-2587 ◽  
Author(s):  
F Collins ◽  
MF Schmidt ◽  
PB Guthrie ◽  
SB Kater
Keyword(s):  
Intracellular Calcium ◽  
Neuronal Survival ◽  
Sustained Increase

Morphology and behaviour of dinoflagellate chromosomes during the cell cycle and mitosis

2000 ◽  
Vol 113 (7) ◽  
pp. 1231-1239 ◽  
Author(s):  
Y. Bhaud ◽  
D. Guillebault ◽  
J. Lennon ◽  
H. Defacque ◽  
M.O. Soyer-Gobillard ◽  
...  
Keyword(s):  
Electron Microscopy ◽  
Cell Cycle ◽  
Confocal Microscopy ◽  
Nuclear Envelope ◽  
Chromosome Segregation ◽  
Morphological Changes ◽  
S Phase ◽  
Chromosome Behaviour ◽  
Double Number ◽  
Do So

The morphology and behaviour of the chromosomes of dinoflagellates during the cell cycle appear to be unique among eukaryotes. We used synchronized and aphidicolin-blocked cultures of the dinoflagellate Crypthecodinium cohnii to describe the successive morphological changes that chromosomes undergo during the cell cycle. The chromosomes in early G(1) phase appeared to be loosely condensed with numerous structures protruding toward the nucleoplasm. They condensed in late G(1), before unwinding in S phase. The chromosomes in cells in G(2) phase were tightly condensed and had a double number of arches, as visualised by electron microscopy. During prophase, chromosomes elongated and split longitudinally, into characteristic V or Y shapes. We also used confocal microscopy to show a metaphase-like alignment of the chromosomes, which has never been described in dinoflagellates. The metaphase-like nucleus appeared flattened and enlarged, and continued to do so into anaphase. Chromosome segregation occurred via binding to the nuclear envelope surrounding the cytoplasmic channels and microtubule bundles. Our findings are summarized in a model of chromosome behaviour during the cell cycle.

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