Uniquely identifying cell orientation and sarcomere length in the intact rodent heart with oblique plane remote focussing microscopy

Author(s):  
A. D. Corbett ◽  
R. A. B. Burton ◽  
G. Bub ◽  
T. Wilson
2013 ◽  
Vol 113 (7) ◽  
pp. 863-870 ◽  
Author(s):  
Edward J. Botcherby ◽  
Alex Corbett ◽  
Rebecca A.B. Burton ◽  
Chris W. Smith ◽  
Christian Bollensdorff ◽  
...  

Author(s):  
G.E. Adomian ◽  
L. Chuck ◽  
W.W. Pannley

Sonnenblick, et al, have shown that sarcomeres change length as a function of cardiac muscle length along the ascending portion of the length-tension curve. This allows the contractile force to be expressed as a direct function of sarcomere length. Below L max, muscle length is directly related to sarcomere length at lengths greater than 85% of optimum. However, beyond the apex of the tension-length curve, i.e. L max, a disparity occurs between cardiac muscle length and sarcomere length. To account for this disproportionate increase in muscle length as sarcomere length remains relatively stable, the concept of fiber slippage was suggested as a plausible explanation. These observations have subsequently been extended to the intact ventricle.


2021 ◽  
Vol 4 (1) ◽  
Author(s):  
Lei Qin ◽  
Xuekun Fu ◽  
Jing Ma ◽  
Manxia Lin ◽  
Peijun Zhang ◽  
...  

AbstractOsteocytes act as mechanosensors in bone; however, the underlying mechanism remains poorly understood. Here we report that deleting Kindlin-2 in osteocytes causes severe osteopenia and mechanical property defects in weight-bearing long bones, but not in non-weight-bearing calvariae. Kindlin-2 loss in osteocytes impairs skeletal responses to mechanical stimulation in long bones. Control and cKO mice display similar bone loss induced by unloading. However, unlike control mice, cKO mice fail to restore lost bone after reloading. Osteocyte Kindlin-2 deletion impairs focal adhesion (FA) formation, cytoskeleton organization and cell orientation in vitro and in bone. Fluid shear stress dose-dependently increases Kindlin-2 expression and decreases that of Sclerostin by downregulating Smad2/3 in osteocytes; this latter response is abolished by Kindlin-2 ablation. Kindlin-2-deficient osteocytes express abundant Sclerostin, contributing to bone loss in cKO mice. Collectively, we demonstrate an indispensable novel role of Kindlin-2 in maintaining skeletal responses to mechanical stimulation by inhibiting Sclerostin expression during osteocyte mechanotransduction.


1992 ◽  
Vol 232 (1) ◽  
pp. 78-84 ◽  
Author(s):  
Theo M. G. J. van Eijden ◽  
Maarten C. Raadsheer

1999 ◽  
Vol 57 (2) ◽  
pp. 144-152 ◽  
Author(s):  
Casey A. Kindig ◽  
David C. Poole

2012 ◽  
Vol 142 (5) ◽  
pp. S-903
Author(s):  
Ravinder K. Mittal ◽  
Bikram Padda ◽  
Mahadevan R. Rajasekaran

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