Intercellular Junctions Play an Important Role in Orientation of Vascular Endothelial Cells Exposed to Cyclic Stretch

2011 ◽  
Author(s):  
Wenjing Huang ◽  
Naoya Sakamoto ◽  
Kazuhiko Hanamura ◽  
Ryotaro Miyazawa ◽  
Masaaki Sato
Keyword(s):  
Signal Transduction ◽  
Endothelial Cells ◽  
Focal Adhesion Kinase ◽  
Focal Adhesion ◽  
Vascular Endothelial Cells ◽  
Intercellular Junctions ◽  
Cyclic Stretch ◽  
Signal Transduction Pathways ◽  
Vascular Endothelial ◽  
Morphological Response

Endothelial cells (ECs) undergoing cyclic stretch align perpendicularly to the stretch direction [1]. Phosphorylation of focal adhesion kinase (FAK), an important component of focal adhesion (FA) signaling pathways, is thought to be required for the stretch-dependent morphological response of ECs [1]. However, since it has been reported that FAK is not always required for EC response to cyclic stretch is regulated by multiple signal transduction pathways in ECs.

Heterogeneity of the signal transduction pathways for VEGF-induced MAPKs activation in human vascular endothelial cells

2001 ◽  
Vol 188 (2) ◽  
pp. 201-210 ◽  
Author(s):  
Rei Yashima ◽  
Mayumi Abe ◽  
Katsuhiro Tanaka ◽  
Hikaru Ueno ◽  
Kenya Shitara ◽  
...  
Keyword(s):  
Signal Transduction ◽  
Endothelial Cells ◽  
Vascular Endothelial Cells ◽  
Signal Transduction Pathways ◽  
Vascular Endothelial

Signal transduction pathways of bacterial lipopolysaccharide-stimulated bovine vascular endothelial cells

Inflammation ◽  
1994 ◽  
Vol 18 (2) ◽  
pp. 221-233 ◽  
Author(s):  
Zhengang Yang ◽  
Philip N. Bochsler ◽  
Roger C. Carroll ◽  
Candace D. Carter ◽  
Lajwanti S. Khemlani ◽  
...  
Keyword(s):  
Signal Transduction ◽  
Endothelial Cells ◽  
Vascular Endothelial Cells ◽  
Bacterial Lipopolysaccharide ◽  
Signal Transduction Pathways ◽  
Vascular Endothelial

scholarly journals Stretch-induced phosphorylation of focal adhesion kinase in endothelial cells: role of mitochondrial oxidants

2006 ◽  
Vol 291 (1) ◽  
pp. L38-L45 ◽  
Author(s):  
Mir H. Ali ◽  
Paul T. Mungai ◽  
Paul T. Schumacker
Keyword(s):  
Signal Transduction ◽  
Endothelial Cells ◽  
Focal Adhesion Kinase ◽  
Signaling Pathway ◽  
Focal Adhesion ◽  
Cyclic Strain ◽  
Cytoskeletal Proteins ◽  
Cyclic Stretch ◽  
Mitochondrial Inhibitors ◽  
Mitochondrial Ros

Mechanical stretch activates a number of signaling pathways in endothelial cells, and it elicits a variety of functional responses including increases in the phosphorylation of focal adhesion kinase (FAK), a nonreceptor tyrosine kinase involved in integrin-mediated signal transduction. Stretch also triggers an increase in the generation of reactive oxygen species (ROS), which may function as second messengers in the signal transduction cascades that activate cellular responses to strain. Mitochondria represent an important source of ROS in the cell, and these organelles may release ROS in response to strain by virtue of their attachment to cytoskeletal proteins. We therefore tested whether cyclic stretch increases FAK phosphorylation at Tyr397 through a mitochondrial ROS signaling pathway in bovine pulmonary artery endothelial cells (BPAEC). Oxidant signaling, measured using 2′7′-dichlorofluorescin (DCFH), increased 152 ± 16% during 1.5 h of cyclic strain relative to unstrained controls. The mitochondrial inhibitors diphenylene iodonium (5 μM) or rotenone (2 μM) attenuated this increase, whereas l-nitroarginine (100 μM), allopurinol (100 μM), or apocynin (30 μM) had no effect. The antioxidants ebselen (5 μM) and dithiodidiethyldithiocarbamate (1 mM) inhibited the strain-induced increase in oxidant signaling, but Hb (5 μM) had no effect. These results indicate that strain induces oxidant release from mitochondria. Treatment with cytochalasin D (5 μM) abrogated strain-induced DCFH oxidation in BPAEC, indicating that actin filaments were required for stretch-induced mitochondrial ROS generation. Cyclic strain increased FAK phosphorylation at Tyr397, but this was abolished by mitochondrial inhibitors as well as by antioxidants. Strain-induced FAK phosphorylation was abrogated by inhibition of protein kinase C (PKC) with Ro-31-8220 or Gö-6976. These findings indicate that mitochondrial oxidants generated in response to endothelial strain trigger FAK phosphorylation through a signaling pathway that involves PKC.

Signal Transduction of Vascular Endothelial Cells

1995 ◽  
Vol 6 (2) ◽  
pp. 67-73
Author(s):  
Michihiko KUWANO ◽  
Hiroto IZUMI ◽  
Tadahisa SHONO ◽  
Sei-ichiro JIMI ◽  
Yukihiro WAKABAYASHI ◽  
...  
Keyword(s):  
Signal Transduction ◽  
Endothelial Cells ◽  
Vascular Endothelial Cells ◽  
Vascular Endothelial
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