Cellular and Molecular Effects of Mechanical Stretch on Vascular Cells

2010 ◽  
pp. 193-217
Author(s):  
Kou-Gi Shyu
Keyword(s):  
Mechanical Stretch ◽  
Vascular Cells ◽  
Molecular Effects

Cellular and molecular effects of mechanical stretch on vascular cells and cardiac myocytes

2009 ◽  
Vol 116 (5) ◽  
pp. 377-389 ◽  
Author(s):  
Kou-Gi Shyu
Keyword(s):  
Shear Stress ◽  
Cardiovascular Diseases ◽  
Cardiovascular System ◽  
Cardiac Myocytes ◽  
Molecular Mechanisms ◽  
Atherosclerotic Lesion ◽  
Mechanical Stretch ◽  
Vascular Cells ◽  
Molecular Effects ◽  
The Impact

Cells in the cardiovascular system are permanently subjected to mechanical forces due to the pulsatile nature of blood flow and shear stress, created by the beating heart. These haemodynamic forces play an important role in the regulation of vascular development, remodelling, wound healing and atherosclerotic lesion formation. Mechanical stretch can modulate several different cellular functions in VSMCs (vascular smooth muscle cells). These functions include, but are not limited to, cell alignment and differentiation, migration, survival or apoptosis, vascular remodelling, and autocrine and paracrine functions. Laminar shear stress exerts anti-apoptotic, anti-atherosclerotic and antithrombotic effects on ECs (endothelial cells). Mechanical stretch of cardiac myocytes can modulate growth, apoptosis, electric remodelling, alterations in gene expression, and autocrine and paracrine effects. The aim of the present review is primarily to summarize the cellular and molecular effects of mechanical stretch on vascular cells and cardiac myocytes, emphasizing the molecular mechanisms underlying the regulation. Knowledge of the impact of mechanical stretch on the cardiovascular system is vital to the understanding of the pathogenesis of cardiovascular diseases, and is also crucial to provide new insights into the prevention and therapy of cardiovascular diseases.

QUASI-MOLECULAR EFFECTS IN ION-ATOM COLLISIONS AT ION ENERGIES IN THE HUNDRED-keV REGION

1979 ◽  
Vol 40 (C1) ◽  
pp. C1-246-C1-249
Author(s):  
E. G. Bøving ◽  
K. Edlund ◽  
G. Sørensen
Keyword(s):  
Ion Energies ◽  
Molecular Effects

How do cardiomyocytes sense stretch? Effects of cyclic mechanical stretch on cardiomyocyte cellular organization

2014 ◽  
Vol 62 (S 01) ◽  
Author(s):  
S. Dhein ◽  
A. Schreiber ◽  
S. Steinbach ◽  
M. Kostelka ◽  
F.W. Mohr
Keyword(s):  
Mechanical Stretch ◽  
Cellular Organization

Thrombin Augments Vascular Cell-dependent Migration of Human Mast Cells: Role of MGF

1997 ◽  
Vol 77 (03) ◽  
pp. 577-584 ◽  
Author(s):  
Mehrdad Baghestanian ◽  
Roland Hofbauer ◽  
Hans G Kress ◽  
Johann Wojta ◽  
Astrid Fabry ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Mast Cells ◽  
Umbilical Vein ◽  
Vascular Cells ◽  
Migratory Response ◽  
Thrombin Activation ◽  
Umbilical Vein Endothelial Cells ◽  
Primary Tissue ◽  
Local Expression

SummaryRecent data suggest that auricular thrombosis is associated with accumulation of mast cells (MC) in the upper endocardium (where usually no MC reside) and local expression of MGF (mast cell growth factor) (25). In this study, the role of vascular cells, thrombin-activation and MGF, in MC-migration was analyzed. For this purpose, cultured human auricular endocardial cells (HAUEC), umbilical vein endothelial cells (HUVEC) and uterine-(HUTMEC) and skin-derived (HSMEC) microvascular endothelial cells were exposed to thrombin or control medium, and the migration of primary tissue MC (lung, n = 6) and HMC-1 cells (human MC-line) against vascular cells (supernatants) measured. Supernatants (24 h) of unstimulated vascular cells (monolayers of endocardium or endothelium) as well as recombinant (rh) MGF induced a significant migratory response in HMC-1 (control: 3025 ± 344 cells [100 ± 11.4%] vs. MGF, 100 ng/ml: 8806 ± 1019 [291 ± 34%] vs. HAUEC: 9703 ± 1506 [320.8 ± 49.8%] vs. HUTMEC: 8950 ± 1857 [295.9 ± 61.4%] vs. HSMEC: 9965 ± 2018 [329.4 ± 66.7%] vs. HUVEC: 9487 ± 1402 [313.6 ± 46.4%], p <0.05) as well as in primary lung MC. Thrombin-activation (5 U/ml, 12 h) of vascular cells led to an augmentation of the directed migration of MC as well as to a hirudin-sensitive increase in MGF synthesis and release. Moreover, a blocking anti-MGF antibody was found to inhibit MC-migration induced by unstimulated or thrombin-activated vascular cells. Together, these data show that endocardial and other vascular cells can induce migration of human MC. This MC-chemotactic signal of the vasculature is associated with expression and release of MGF, augmentable by thrombin, and may play a role in the pathophysiology of (auricular) thrombosis.

The cellular and molecular effects of the androgen receptor agonist, Cl-4AS-1, on breast cancer cells

2016 ◽  
Author(s):  
Mamoun Ahram ◽  
Ebtihal Mustafa ◽  
Shatha Abu Hammad ◽  
Mariam Hodhod ◽  
Malek Zihlif
Keyword(s):  
Breast Cancer ◽  
Androgen Receptor ◽  
Cancer Cells ◽  
Receptor Agonist ◽  
Breast Cancer Cells ◽  
Molecular Effects
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