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TLE4 Is a Critical Mediator of Osteoblast and Runx2-Dependent Bone Development
Healthy bone homeostasis hinges upon a delicate balance and regulation of multiple processes that contribute to bone development and metabolism. While examining hematopoietic regulation by , we have uncovered a previously unappreciated role of on bone calcification using a novel null mouse model. Gi...
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Published in: | Frontiers in cell and developmental biology 2021-08, Vol.9, p.671029-671029 |
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Main Authors: | , , , , , , |
Format: | Article |
Language: | English |
Subjects: | |
Citations: | Items that this one cites Items that cite this one |
Online Access: | Get full text |
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Summary: | Healthy bone homeostasis hinges upon a delicate balance and regulation of multiple processes that contribute to bone development and metabolism. While examining hematopoietic regulation by
, we have uncovered a previously unappreciated role of
on bone calcification using a novel
null mouse model. Given the significance of osteoblasts in both hematopoiesis and bone development, this study investigated how loss of
affects osteoblast function. We used dynamic bone formation parameters and microCT to characterize the adverse effects of
loss on bone development. We further demonstrated loss of
impacts expression of several key osteoblastogenic genes, including
,
, and
, pointing toward a potential novel mechanism for
-dependent regulation of mammalian bone development in collaboration with the RUNX family members. |
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ISSN: | 2296-634X 2296-634X |
DOI: | 10.3389/fcell.2021.671029 |