scholarly journals A mathematical model of the cytosolic-free calcium response in endothelial cells to fluid shear stress

1997 ◽  
Vol 94 (8) ◽  
pp. 3726-3731 ◽  
Author(s):  
T. F. Wiesner ◽  
B. C. Berk ◽  
R. M. Nerem
Keyword(s):  
Mathematical Model ◽  
Endothelial Cells ◽  
Shear Stress ◽  
Fluid Shear Stress ◽  
Free Calcium ◽  
Fluid Shear ◽  
Cytosolic Free Calcium ◽  
Calcium Response

Fluid shear stress modulates cytosolic free calcium in vascular endothelial cells

1992 ◽  
Vol 262 (2) ◽  
pp. C384-C390 ◽  
Author(s):  
J. Shen ◽  
F. W. Luscinskas ◽  
A. Connolly ◽  
C. F. Dewey ◽  
M. A. Gimbrone
Keyword(s):  
Endothelial Cells ◽  
Shear Stress ◽  
Fluid Shear Stress ◽  
Vascular Endothelial Cells ◽  
Free Calcium ◽  
Fluid Shear ◽  
Aortic Endothelial Cells ◽  
High K ◽  
Applied Shear Stress ◽  
Agonist Concentration

Cytosolic free Ca2+ concentration ([Ca2+]i) was monitored in single and groups of fura-2-loaded bovine aortic endothelial cells (BAEC) during exposure to laminar fluid shear stress. Application of a step increase in shear stress from 0.08 to 8 dyn/cm2 to confluent BAEC monolayers resulted in a transient increase in [Ca2+]i, which attained a peak value in 15-40 s, followed by a decline to baseline within 40-80 s. The magnitude of the [Ca2+]i responses increased with applied shear stress over the range of 0.2-4 dyn/cm2 and reached a maximum at greater than 4 dyn/cm2. Transient oscillations in [Ca2+]i with gradually diminishing amplitude were observed in individual cells subjected to continuous high shear stress. Elimination of extracellular Ca2+ with ethylene glycol-bis(beta-aminoethyl ether)-N,N,N',N'-tetraacetic acid, blockade of Ca2+ entry with lanthanum, depolarization of the cell membrane with high K+, and preconditioning of BAEC in steady laminar flow had little effect on the [Ca2+]i response. In the presence of ATP or ADP, application of shear stress caused repetitive oscillations in [Ca2+]i in single BAEC, whose frequency was dependent on both agonist concentration and the magnitude of applied shear stress. However, apyrase, an ATPase and ADPase, did not inhibit the shear-induced [Ca2+]i responses in standard medium (no added ATP or ADP), suggesting that the shear-induced [Ca2+]i response is not due to ATP released by endothelial cells.

scholarly journals Lepasnya Sel Endotel Dan Vascular Endothelial Cadherin (Ve-Cadherin) Pada Huvecs Dengan Glukosa Tinggi Dan Fluid Shear Stress

2020 ◽  
Vol 8 (2) ◽  
pp. 92
Author(s):  
Yoyon Arif ◽  
Erna Sulistiowati
Keyword(s):  
Endothelial Cells ◽  
Shear Stress ◽  
Fluid Shear Stress ◽  
Vascular Endothelial ◽  
Fluid Shear ◽  
Vascular Endothelial Cadherin

Sel endotel melapisi lumen pembuluh darah sehingga menyebabkan paparan langsung aliran darah dan timbul gaya hemodinamik shear stress. Vascular Endothelial (VE) Cadherin merupakan salah satu struktur penghubung antar sel yang berperan mencegah terlepasnya sel endotel dari membran dasar. Paparan glukosa tinggi menyebabkan stress oksidatif sehingga sel endotel mengalami apoptosis dan nekrosis dan terlepas. Penelitian ini bertujuan mempelajari efek paparan glukosa tinggi dan fluid shear stress terhadap morfologi, struktur VE-Cadherin dan densitas sel endotel pada kultur sel endotel HUVECs (Human Vein Endothelial Cells Culture).Metode Penelitian eksperimental laboratorium dengan  metode HUVECs yang dipapar d-glukosa 22 mM selama 7 hari. Shear stress dibangkitkan dengan alat cone and plate 10 dyne/cm2 selama 5, 8, 12 dan 15 menit. Pulasan VE-Cadherin dengan imunohistokimia. Data dianalisis dengan metode statistik. Signifikan pada p<0,05.Hasil Shear stress selama 15 menit menyebabkan perubahan bentuk sel endotel  menjadi lebih panjang dan inti sel lebih pipih. Paparan glukosa tinggi dan fluid shear stress menyebabkan penurunan skor VE-Cadherin dan densitas sel endotel secara signifikan Penurunan skor VE-Cadherin berpengaruh langsung terhadap penurunan densitas sel endotel.Kesimpulan. Paparan glukosa tinggi dan fluid shear stress menyebabkan kerusakan struktur VE-Cadherin sehingga terjadi peningkatan apoptosis dan nekrosis sel endotel.

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