TLE4 Is a Critical Mediator of Osteoblast and Runx2-Dependent Bone Development.

Front Cell Dev Biol

Department of Pediatrics, Center of Genomic Medicine, Divisions of Pediatric Hematology/Oncology and Medical Genetics, Massachusetts General Hospital, Harvard Medical School, Boston, MA, United States.

Published: August 2021

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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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8377417PMC
http://dx.doi.org/10.3389/fcell.2021.671029DOI Listing

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