Calcium Efflux From Bone Matrix in Response to Mechanical Loading

2011 ◽  
Author(s):  
Xuanhao Sun ◽  
Eric S. McLamore ◽  
D. Marshall Porterfield ◽  
Ozan Akkus
Keyword(s):  
Hydrostatic Pressure ◽  
Cell Surface ◽  
Bone Cells ◽  
Bone Matrix ◽  
Mechanical Stimulus ◽  
Calcium Efflux ◽  
Fluid Shear ◽  
Mechanical Environment ◽  
Surface Receptors ◽  
Cellular Events

Bone is known for its ability to self-repair the microdamage and actively adapt to its mechanical environment, both of which are under the coordination of bone cells. Mechanical cues are sensed by cells and converted into cellular events in a process called mechanotransduction [1]. Most theories of mechanotransduction are based on direct stimulus of cell surface receptors by substrate deformation, fluid shear and/or hydrostatic pressure [2]. Yet, mechanical stimulus may come to affect cell response indirectly, via pathways which alter the pericellular niche. Such indirect pathways of mechanotransduction are not well-investigated for bone.

Mechanically Induced Calcium Release From Bone Matrix Triggers Intracellular Ca2+ Signalling in Osteoblasts: A Novel Mechanotransduction Mechanism

2011 ◽  
Author(s):  
Xuanhao Sun ◽  
Vipuil Kishore ◽  
Kateri Fites ◽  
Ozan Akkus
Keyword(s):  
Fluid Flow ◽  
Hydrostatic Pressure ◽  
Calcium Release ◽  
Bone Cells ◽  
Bone Matrix ◽  
Bone Adaptation ◽  
Exact Form ◽  
Flow Shear ◽  
Damage Repair ◽  
Physical Stimuli

Bone cells are responsible for sensing and converting the mechanical signals into cellular signals to drive bone adaptation and damage repair [1]. Cell-mediated repair of bone is reported to be in preferential association with regions filled with microdamage [2]. Although different theories have been proposed for mechanisms involved in those processes (such as substrate deformation, fluid flow shear, and hydrostatic pressure in mechanotransduction [3], or microcrack and osteocyte apoptosis in damage detection [4]), knowledge on the exact form of physical stimuli which trigger bone cells, especially in critically loaded regions of bone, is still elusive.

scholarly journals Insulin’s Discovery: New Insights on Its Hundredth Birthday: From Insulin Action and Clearance to Sweet Networks

2021 ◽  
Vol 22 (3) ◽  
pp. 1030
Author(s):  
Melanie Leroux ◽  
Martial Boutchueng-Djidjou ◽  
Robert Faure
Keyword(s):  
Type 1 Diabetes ◽  
Cell Surface ◽  
20Th Century ◽  
Insulin Action ◽  
100Th Anniversary ◽  
The Body ◽  
Nobel Lecture ◽  
Surface Receptors ◽  
The Third

In 2021, the 100th anniversary of the isolation of insulin and the rescue of a child with type 1 diabetes from death will be marked. In this review, we highlight advances since the ingenious work of the four discoverers, Frederick Grant Banting, John James Rickard Macleod, James Bertram Collip and Charles Herbert Best. Macleoad closed his Nobel Lecture speech by raising the question of the mechanism of insulin action in the body. This challenge attracted many investigators, and the question remained unanswered until the third part of the 20th century. We summarize what has been learned, from the discovery of cell surface receptors, insulin action, and clearance, to network and precision medicine.

scholarly journals Cell Surface Receptors: Rapid Quantification of Live Cell Receptors Using Bioluminescence in a Flow-Based Microfluidic Device (Small 8/2015)

Small ◽  
2015 ◽  
Vol 11 (8) ◽  
pp. 1012-1012
Author(s):  
Ramesh Ramji ◽  
Cheong Fook Cheong ◽  
Hiroaki Hirata ◽  
Abdur Rub Abdur Rahman ◽  
Chwee Teck Lim
Keyword(s):  
Cell Surface ◽  
Microfluidic Device ◽  
Live Cell ◽  
Cell Surface Receptors ◽  
Cell Receptors ◽  
Surface Receptors ◽  
Rapid Quantification

Inhibition of rat ventricular automaticity by adenosine

1985 ◽  
Vol 248 (6) ◽  
pp. H907-H913 ◽  
Author(s):  
L. J. Heller ◽  
R. A. Olsson
Keyword(s):  
Cell Surface ◽  
Cell Surface Receptor ◽  
Chronotropic Effect ◽  
Surface Receptors ◽  
Adenosine Concentration ◽  
Surface Receptor ◽  
Ventricular Automaticity ◽  
Beating Rate ◽  
Chronotropic Effects ◽  
Developed Pressure

This study was designed to characterize adenosine's negative chronotropic effect on ventricular pacemakers. The spontaneous beating rate of isolated, isovolumic rat ventricular preparations perfused with Krebs-Henseleit solution decreased as the adenosine concentration was increased [log M effective concentration 50% (EC50) = -5.22 +/- 0.17]. The lack of effect of propranolol or atropine on this adenosine response eliminates the involvement of endogenous neurotransmitters. Support for the involvement of an external cell surface receptor was provided by findings that theophylline and 8-(4-sulfophenyl)theophylline, an analogue thought to act solely at the cell surface, significantly increased the adenosine log M EC50 to -3.94 +/- 0.22 and -3.61 +/- 0.22, respectively. An increase in spontaneous beating rate induced by theophylline, but not by its analogue, was blocked by the addition of propranolol. The relative chronotropic potency of the adenosine analogues R-PIA, S-PIA, and NECA suggests that the cell surface receptors may be of the Ri type. The negative chronotropic effects of adenosine and its analogues occurred at concentrations that had no effect on the developed pressure of the paced preparation. Electrocardiographic evaluations indicate that at high agonist concentrations, there was an abrupt alteration in electrical properties of the preparation, which could be blocked by theophylline and its analogue.

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