scholarly journals Energy metabolism of intervertebral disc under mechanical loading

2013 ◽  
Vol 31 (11) ◽  
pp. 1733-1738 ◽  
Author(s):  
Chong Wang ◽  
Silvia Gonzales ◽  
Howard Levene ◽  
Weiyong Gu ◽  
Chun-Yuh Charles Huang
2011 ◽  
Vol 29 (11) ◽  
pp. 1634-1641 ◽  
Author(s):  
Hanan N. Fernando ◽  
Jessica Czamanski ◽  
Tai-Yi Yuan ◽  
Weiyong Gu ◽  
Abdi Salahadin ◽  
...  

Author(s):  
Sheng-Long Ding ◽  
Tai-Wei Zhang ◽  
Qi-Chen Zhang ◽  
Wang Ding ◽  
Ze-Fang Li ◽  
...  

AbstractNight shift workers with disordered rhythmic mechanical loading are more prone to intervertebral disc degeneration (IDD). Our results showed that circadian rhythm (CR) was dampened in degenerated and aged NP cells. Long-term environmental CR disruption promoted IDD in rats. Excessive mechanical strain disrupted the CR and inhibited the expression of core clock proteins. The inhibitory effect of mechanical loading on the expression of extracellular matrix genes could be reversed by BMAL1 overexpression in NP cells. The Rho/ROCK pathway was demonstrated to mediate the effect of mechanical stimulation on CR. Prolonged mechanical loading for 12 months affected intrinsic CR genes and induced IDD in a model of upright posture in a normal environment. Unexpectedly, mechanical loading further accelerated the IDD in an Light-Dark (LD) cycle-disrupted environment. These results indicated that intrinsic CR disruption might be a mechanism involved in overloading-induced IDD and a potential drug target for night shift workers.


2018 ◽  
Vol 26 (7) ◽  
pp. 978-987 ◽  
Author(s):  
S.E. Navone ◽  
M. Peroglio ◽  
L. Guarnaccia ◽  
M. Beretta ◽  
S. Grad ◽  
...  

2000 ◽  
Vol 122 (3) ◽  
pp. 245-251 ◽  
Author(s):  
Anthony E. Baer ◽  
Lori A. Setton

Cells of the intervertebral disc exhibit spatial variations in phenotype and morphology that may be related to differences in their local mechanical environments. In this study, the stresses, strains, and dilatations in and around cells of the intervertebral disc were studied with an analytical model of the cell as a mechanical inclusion embedded in a transversely isotropic matrix. In response to tensile loading of the matrix, the local mechanical environment of the cell differed among the anatomic regions of the disc and was strongly influenced by changes in both matrix anisotropy and parameters of cell geometry. The results of this study suggest that the local cellular mechanical environment may play a role in determining both cell morphology in situ and the inhomogeneous response to mechanical loading observed in cells of the disc. [S0148-0731(00)00603-8]


2021 ◽  
Vol 22 (16) ◽  
pp. 9070
Author(s):  
Shu Somemura ◽  
Takanori Kumai ◽  
Kanaka Yatabe ◽  
Chizuko Sasaki ◽  
Hiroto Fujiya ◽  
...  

Mechanical stress is an important factor affecting bone tissue homeostasis. We focused on the interactions among mechanical stress, glucose uptake via glucose transporter 1 (Glut1), and the cellular energy sensor sirtuin 1 (SIRT1) in osteoblast energy metabolism, since it has been recognized that SIRT1, an NAD+-dependent deacetylase, may function as a master regulator of the mechanical stress response as well as of cellular energy metabolism (glucose metabolism). In addition, it has already been demonstrated that SIRT1 regulates the activity of the osteogenic transcription factor runt-related transcription factor 2 (Runx2). The effects of mechanical loading on cellular activities and the expressions of Glut1, SIRT1, and Runx2 were evaluated in osteoblasts and chondrocytes in a 3D cell–collagen sponge construct. Compressive mechanical loading increased osteoblast activity. Mechanical loading also significantly increased the expression of Glut1, significantly decreased the expression of SIRT1, and significantly increased the expression of Runx2 in osteoblasts in comparison with non-loaded osteoblasts. Incubation with a Glut1 inhibitor blocked mechanical stress-induced changes in SIRT1 and Runx2 in osteoblasts. In contrast with osteoblasts, the expressions of Glut1, SIRT1, and Runx2 in chondrocytes were not affected by loading. Our present study indicated that mechanical stress induced the upregulation of Glut1 following the downregulation of SIRT1 and the upregulation of Runx2 in osteoblasts but not in chondrocytes. Since SIRT1 is known to negatively regulate Runx2 activity, a mechanical stress-induced downregulation of SIRT1 may lead to the upregulation of Runx2, resulting in osteoblast differentiation. Incubation with a Glut1 inhibitor the blocked mechanical stress-induced downregulation of SIRT1 following the upregulation of Runx2, suggesting that Glut1 is necessary to mediate the responses of SIRT1 and Runx2 to mechanical loading in osteoblasts.


Author(s):  
Yongren Wu ◽  
John Glaser ◽  
Hai Yao

The intervertebral disc (IVD) is the largest cartilaginous structure in human body that contributes to flexibility and load support in the spine. To accomplish these functions, the disc has a unique architecture consisting of a centrally-located nucleus pulposus (NP) surrounded superiorly and inferiorly by cartilage endplates (CEP) and peripherally by the annulus fibrosus (AF). Disc degeneration is strongly linked to low back pain. Poor nutrient supply has been suggested as a potential mechanism for disc degeneration. Previous theoretical studies have shown that the distributions of nutrients and metabolites (e.g., oxygen, glucose, and lactate) within the IVD depended on tissue diffusivities, nutrient supply, and cellular metabolic rates [1, 2]. Based on a multiphasic mechano-electrochemical finite element model of human IVD [3], our recent theoretical study suggested that the mechanical loading has little effect on small solute transport (e.g., glucose), but significantly affects large solute transport (e.g., growth factor). The objective of this study was to further develop the multiphasic finite element model of IVD by including the cartilage endplate and considering the nutrient consumption of disc cells. Using this model, the effects of endplate and mechanical loading on solute transport in IVD were examined.


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