Aurora Kinase A Regulates Cell Transitions in Glucocorticoid-Induced Bone Loss

Author:

Qiao Xiaojing1,Yang Yang1,Zhao Yan1,Wu Xiuju1ORCID,Zhang Li1,Cai Xinjiang1ORCID,Ji Jaden1,Boström Kristina I.12,Yao Yucheng1

Affiliation:

1. Division of Cardiology, David Geffen School of Medicine at UCLA, Los Angeles, CA 90095-1679, USA

2. The Molecular Biology Institute at UCLA, Los Angeles, CA 90095-1570, USA

Abstract

Glucocorticoid-induced bone loss is a severe and toxic effect of long-term therapy with glucocorticoids, which are currently prescribed for millions of people worldwide. Previous studies have uncovered that glucocorticoids reciprocally converted osteoblast lineage cells into endothelial-like cells to cause bone loss and showed that the modulations of Foxc2 and Osterix were the causative factors that drove this harmful transition of osteoblast lineage cells. Here, we find that the inhibition of aurora kinase A halts this transition and prevents glucocorticoid-induced bone loss. We find that aurora A interacts with the glucocorticoid receptor and show that this interaction is required for glucocorticoids to modulate Foxc2 and Osterix. Together, we identify a new potential approach to counteracting unwanted transitions of osteoblast lineage cells in glucocorticoid treatment and may provide a novel strategy for ameliorating glucocorticoid-induced bone loss.

Funder

NIH

Publisher

MDPI AG

Subject

General Medicine

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