scholarly journals Fluid Shear-stress Increases TRPV4-Expression in Human Endothelial Cells in an Experimental in Vitro Model

2019 ◽  
Vol 58 (6) ◽  
pp. e717
Author(s):  
Thomas Schmandra ◽  
Rita Al Weissi ◽  
Kerstin Troidl ◽  
Thomas Schmitz-Rixen
1994 ◽  
Vol 205 (2) ◽  
pp. 1345-1352 ◽  
Author(s):  
Y. Takada ◽  
F. Shinkai ◽  
S. Kondo ◽  
S. Yamamoto ◽  
H. Tsuboi ◽  
...  

2000 ◽  
Vol 87 (5) ◽  
pp. 385-391 ◽  
Author(s):  
Kimiko Yamamoto ◽  
Risa Korenaga ◽  
Akira Kamiya ◽  
Joji Ando

2000 ◽  
Vol 20 (3) ◽  
pp. 617-623 ◽  
Author(s):  
Boris-Wolfgang Hochleitner ◽  
Elisabeth-Olga Hochleitner ◽  
Peter Obrist ◽  
Thomas Eberl ◽  
Albert Amberger ◽  
...  

Author(s):  
Jeffrey A. Kornuta ◽  
Arina Korneva ◽  
J. Brandon Dixon

Nearly all tissues are supported by the lymphatic system for a variety of functions, including the regulation of fluid balance, the removal of particulate matter from the interstitium, as well as the transport of fat from the intestine to the blood, among others. Despite these important functions, very little is known about the particular mechanisms through which the lymphatics fulfill these roles. Lymphedema, a chronic disease characterized by an inability of the lymphatics to maintain tissue homeostasis and estimated to affect over 130 million people worldwide, can result in serious clinical problems for which there are very few beneficial cures or therapies [1]. While fluid stagnation is the primary clinical manifestation of the disease, severe lymphedema is often correlated with tissue remodeling and the gross accumulation of lipid [1]. Given these symptoms, one must consider the breakdown in the lymphatic response to mechanical load (i.e. fluid balance) in order to understand the progression of the disease.


1998 ◽  
Vol 31 ◽  
pp. 173 ◽  
Author(s):  
O. Boutherin Falson ◽  
C. Haond ◽  
M. Chaslon ◽  
M. Moenner ◽  
S. Naili ◽  
...  

2015 ◽  
Vol 65 (5) ◽  
pp. 508-515 ◽  
Author(s):  
Stefan Dhein ◽  
Alice Wermke ◽  
Sandy von Salisch ◽  
Franziska Schlegel ◽  
Holger Stepan ◽  
...  

2020 ◽  
Vol 245 (18) ◽  
pp. 1656-1663
Author(s):  
Junyao Wang ◽  
Shiyanjin Zhang

Mechanosensitive genes regulate multiple cardiovascular pathophysiological processes and disorders; however, the role of flow-sensitive genes in atherosclerosis is still unknown. In this study, we identify LIM Zinc Finger Domain Containing 2 (LIMS2) that acts as a mechanosensitive gene downregulated by disturbed flow (d-flow) both in human endothelial cells (ECs) in vitro and in mice in vivo. Mechanistically, d-flow suppresses LIMS2 expression, which leads to endothelial inflammation by upregulating typical inflammatory factors, VCAM-1, and ICAM-1 in human ECs. The findings indicate that LIMS2, the new flow-sensitive gene, may help us to find a new insight to explain how d-flow caused endothelial inflammation and provide a new therapeutic approach for atherosclerosis in the future.


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