Nucleus Pulposus Cell Response to Confined and Unconfined Compression Implicates Mechanoregulation by Fluid Shear Stress

2010 ◽  
Vol 39 (3) ◽  
pp. 1101-1111 ◽  
Author(s):  
Ping Wang ◽  
Li Yang ◽  
Adam H. Hsieh
Keyword(s):  
Shear Stress ◽  
Nucleus Pulposus ◽  
Cell Response ◽  
Fluid Shear Stress ◽  
Nucleus Pulposus Cell ◽  
Unconfined Compression ◽  
Fluid Shear

scholarly journals Moderate Fluid Shear Stress Could Regulate the Cytoskeleton of Nucleus Pulposus and Surrounding Inflammatory Mediators by Activating the FAK-MEK5-ERK5-cFos-AP1 Signaling Pathway

2018 ◽  
Vol 2018 ◽  
pp. 1-9 ◽  
Author(s):  
Dongping Ye ◽  
Weiguo Liang ◽  
Libing Dai ◽  
Yicun Yao
Keyword(s):  
Shear Stress ◽  
Signaling Pathway ◽  
Nucleus Pulposus ◽  
Inflammatory Mediators ◽  
Fluid Shear Stress ◽  
Nucleus Pulposus Cell ◽  
Type Ii Collagen ◽  
Type Ii ◽  
Fluid Shear ◽  
Protein Map

We first applied moderate fluid shear stress to nucleus pulposus cells. The correlation of AP-1 with type II collagen, proteoglycan, Cytokeratin 8 protein, MAP-1, MAP-2, and MAP-4 and the correlation of AP-1 with IL-1β, TNF-α, IL-6, IL-8, MIP-1, MCP-1, and NO were detected. Our results document that moderate fluid shear stress could activate the FAK-MEK5-ERK5-cFos-AP1 signaling pathway. AP1 could downregulate the construct factors of cytoskeleton such as type II collagen, proteoglycan, Cytokeratin 8 protein, MAP-1, MAP-2, and MAP-4 in nucleus pulposus cell after the fluid shear stress was loaded. AP1 could upregulate the inflammatory factors such as IL-1β, TNF-α, IL-6, IL-8, MIP-1, MCP-1, and NO in nucleus pulposus cell after the fluid shear stress was loaded. Taken together, our data suggested that moderate fluid shear stress may play an important role in the cytoskeleton of nucleus pulposus and surrounding inflammatory mediators by activating the FAK-MEK5-ERK5-cFos-AP1 signaling pathway, thereby affecting cell degeneration.

A mechanosensory complex that mediates the endothelial cell response to fluid shear stress

Nature ◽  
2005 ◽  
Vol 437 (7057) ◽  
pp. 426-431 ◽  
Author(s):  
Eleni Tzima ◽  
Mohamed Irani-Tehrani ◽  
William B. Kiosses ◽  
Elizabetta Dejana ◽  
David A. Schultz ◽  
...  
Keyword(s):  
Shear Stress ◽  
Endothelial Cell ◽  
Cell Response ◽  
Fluid Shear Stress ◽  
Fluid Shear ◽  
Endothelial Cell Response

T-786C Polymorphism of thenos-3Gene and the Endothelial Cell Response to Fluid Shear Stress—A Proteome Analysis

2009 ◽  
Vol 8 (6) ◽  
pp. 3161-3168 ◽  
Author(s):  
Abdul R. Asif ◽  
Michael Oellerich ◽  
Victor William Armstrong ◽  
Markus Hecker ◽  
Marco Cattaruzza
Keyword(s):  
Shear Stress ◽  
Endothelial Cell ◽  
Cell Response ◽  
Fluid Shear Stress ◽  
Proteome Analysis ◽  
Fluid Shear ◽  
Endothelial Cell Response

scholarly journals MicroRNA-222 regulates fluid shear stress-induced human nucleus pulposus cells degeneration through affecting c-Fos expression

2019 ◽  
Author(s):  
Haixiong Miao ◽  
Yicun Yao ◽  
Baoqing Ye ◽  
Libing Dai ◽  
Weiguo Liang
Keyword(s):  
Shear Stress ◽  
Molecular Mechanism ◽  
Nucleus Pulposus ◽  
Fluid Shear Stress ◽  
Type Ii Collagen ◽  
Cell Counting ◽  
Type Ii ◽  
Fluid Shear ◽  
Nucleus Pulposus Cells

AbstractIntervertebral disc degeneration (IVDD) is a chronic disease that correlates with the deterioration of the nucleus pulposus (NP) cells. However, the molecular mechanism of IVDD remains unclear. In this study, we investigated the function of microRNA-222 in IVDD and the potential molecular mechanism. NP cells treated with fluid shear stress (FSS) were used to simulate a model of IVDD in vitro. MicroRNA-222 was significantly downregulated in NP cells stimulated with FSS compared with that in unstimulated NP cells. Human NP cells were also treated with FSS to induce their degeneration. The mRNA and protein levels of C-FOS, MEK, phosphorylated MEK5 (pMEK5), ERK5, and pERK5 were evaluated with RT-PCR and western blotting, respectively. Enzyme-linked immunosorbent assays were used to investigate type II collagen and Aggrecan expression. NP cell proliferation was determined with the Cell Counting Kit-8. MicroRNA-222 was significantly downregulated in NP cells treated with FSS. The production of c-Fos and MEK5 were markedly reduced or increased in NP cells transfected with the has-microRNA-222 mimic or inhibitor, respectively, whether or not they were stimulated with FSS. The overexpression or inhibition of microRNA-222 markedly accelerated or suppressed the apoptosis of FSS-stimulated NP cells, respectively. In the NP cells, the overexpression or inhibition of microRNA-222 massively inhibited or strengthened Aggrecan and type II collagen expression. Together, our data indicated that c-Fos was a target of microRNA-222, and was negatively regulated by microRNA-222 in NP cells. Our findings also suggested that microRNA-222 is a possible therapeutic target for IVDD because it regulates c-Fos.

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