EurekaMag.com logo
+ Site Statistics
References:
53,869,633
Abstracts:
29,686,251
+ Search Articles
+ Subscribe to Site Feeds
EurekaMag Most Shared ContentMost Shared
EurekaMag PDF Full Text ContentPDF Full Text
+ PDF Full Text
Request PDF Full TextRequest PDF Full Text
+ Follow Us
Follow on FacebookFollow on Facebook
Follow on TwitterFollow on Twitter
Follow on LinkedInFollow on LinkedIn

+ Translate

RANKL and OPG activity is regulated by injury size in networks of osteocyte-like cells



RANKL and OPG activity is regulated by injury size in networks of osteocyte-like cells



Bone 48(2): 182-188



Bone remodelling is an intricate process encompassing numerous paracrine and autocrine biochemical pathways and mechanical mechanisms. It is responsible for maintaining bone homeostasis, structural integrity and function. The RANKL-RANK-OPG cytokine system is one of the principal mediators in the maintenance of bone cell function and activation of bone remodelling by the Basic Multicellular Unit (BMU) which carries out remodelling. Theories surrounding the initiation of bone remodelling include mechanical loading, fluid flow and microdamage as potential stimuli. This study focused on microdamage. In an in vitro simulated bone environment, gel embedded MLO-Y4 cell networks were subjected to damage in the form of planar, crack-like defects of constant area and varying thickness. The biochemical response was determined by ELISA and luciferase assay. The results showed that RANKL release increased and OPG decreased in a manner which depended on injury size (i.e. thickness) and time following application of injury. The effect of microdamage on cell viability and apoptosis was also evaluated. This work demonstrates that injury alone, in the absence of imposed strain or fluid flow, is sufficient to initiate changes in cytokine concentrations of the type which are known to stimulate bone remodeling.

(PDF emailed within 0-6 h: $19.90)

Accession: 055333150

Download citation: RISBibTeXText

PMID: 20854946

DOI: 10.1016/j.bone.2010.09.014



Related references

Osteocyte Apoptosis Caused by Hindlimb Unloading is Required to Trigger Osteocyte RANKL Production and Subsequent Resorption of Cortical and Trabecular Bone in Mice Femurs. Journal of Bone and Mineral Research 31(7): 1356-1365, 2016

Sclerostin stimulates osteocyte support of osteoclast activity by a RANKL-dependent pathway. Plos One 6(10): E25900-E25900, 2012

RANKL expression in myeloma cells is regulated by a network involving RANKL promoter methylation, DNMT1, microRNA and TNFα in the microenvironment. Biochimica et Biophysica Acta 1843(9): 1834-1838, 2014

Effects of high glucose and advanced glycation end products on the expressions of sclerostin and RANKL as well as apoptosis in osteocyte-like MLO-Y4-A2 cells. Biochemical and Biophysical Research Communications 461(2): 193-199, 2015

Osteogenic differentiation of mesenchymal stem cells is regulated by osteocyte and osteoblast cells in a simplified bone niche. European Cells & Materials 23: 13-27, 2012

Osteocyte RANKL: new insights into the control of bone remodeling. Journal of Bone and Mineral Research 27(3): 499-505, 2012

Osteocyte-derived RANKL is a critical mediator of the increased bone resorption caused by dietary calcium deficiency. Bone 66: 146-154, 2015

Runx-2 is not essential for the vitamin D-regulated expression of RANKL and osteoprotegerin in osteoblastic cells. Biochemical and Biophysical Research Communications 324(2): 655-660, 2004

Treatment with anti-RANKL antibody reduces infarct size and attenuates dysfunction impacting on neutrophil-mediated injury. Journal of Molecular and Cellular Cardiology 94: 82-94, 2016

Osteocyte network; a negative regulatory system for bone mass augmented by the induction of Rankl in osteoblasts and Sost in osteocytes at unloading. Plos One 7(6): E40143-E40143, 2012

Estrogen inhibits RANKL-stimulated osteoclastic differentiation of human monocytes through estrogen and RANKL-regulated interaction of estrogen receptor- with BCAR1 and Traf6. Experimental Cell Research 315(7): 1287-1301, 2009

Estrogen inhibits RANKL-stimulated osteoclastic differentiation of human monocytes through estrogen and RANKL-regulated interaction of estrogen receptor-alpha with BCAR1 and Traf6. Experimental Cell Research 315(7): 1287-1301, 2009

Olmesartan decreased levels of IL-1β and TNF-α, down-regulated MMP-2, MMP-9, COX-2, RANK/RANKL and up-regulated SOCs-1 in an intestinal mucositis model. Plos One 9(12): E114923-E114923, 2015

Will personalized medicine help in 'transforming' the business of healthcare?. Personalized Medicine 6(5): 555-565, 2018

Membrane-bound receptor activator of NFκB ligand (RANKL) activity displayed by osteoblasts is differentially regulated by osteolytic factors. Biochemical and Biophysical Research Communications 422(1): 48-53, 2012