English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Plus annual

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Tools annual

Global: Zendy Free Plan

Global: Zendy Tools monthly

Global: Zendy Plus monthly

The integrin α v β 3  has been shown to play an important role in osteocyte mechanotransduction. It has been reported that there are fewer β 3  integrin-containing cells in osteoporotic bone cells. Osteocytes cultured  in vitro  under estrogen deficient conditions demonstrate altered mechanotransduction. However, it is unknown whether the altered mechanotransduction in estrogen deficient osteocytes is directly associated with defective α v β 3  expression or signalling. The objective of this study is to investigate the role of estrogen deficiency for regulating MLO-Y4 cell morphology, α v β 3  expression, focal adhesion formation and mechanotransduction by osteocytes. Here, we report that estrogen withdrawal leads to a smaller focal adhesion area and reduced α v β 3  localisation at focal adhesion sites, resulting in an increased  Rankl / Opg  ratio and defective  Cox-2  responses to oscillatory fluid flow. Interestingly, α v β 3  antagonism had a similar effect on focal adhesion assembly,  Rankl / Opg  ratio, and  Cox-2  responses to oscillatory fluid flow. Taken together, our results provide the first evidence for a relationship between estrogen withdrawal and defective α v β 3 -mediated signalling. Specifically, this study implicates estrogen withdrawal as a putative mechanism responsible for altered α v β 3  expression and resultant changes in downstream signalling in osteocytes during post-menopausal osteoporosis, which might provide an important, but previously unidentified, contribution to the bone loss cascade.

Estrogen deficiency impairs integrin αvβ3-mediated mechanosensation by osteocytes and alters osteoclastogenic paracrine signalling