AI Article Synopsis
- * Researchers found that removing Hem1 from mice led to higher bone mass due to reduced bone resorption, indicating that Hem1 is important for regulating bone density.
- * Hem1-deficient osteoclasts (cells that break down bone) can still form but function poorly, which can be improved by transplanting normal bone marrow cells, highlighting Hem1's key role in bone maintenance.
Article Abstract
Hem1 (hematopoietic protein 1), a hematopoietic cell-specific member of the Hem family of cytoplasmic adaptor proteins, is essential for lymphopoiesis and innate immunity as well as for the transition of hematopoiesis from the fetal liver to the bone marrow. However, the role of Hem1 in bone cell differentiation and bone remodeling is unknown. Here, we show that deletion of Hem1 resulted in a markedly increase in bone mass because of defective bone resorption in mice of both sexes. Hem1-deficient osteoclast progenitors were able to differentiate into osteoclasts, but the osteoclasts exhibited impaired osteoclast fusion and decreased bone-resorption activity, potentially because of decreased mitogen-activated protein kinase and tyrosine kinase c-Abl activity. Transplantation of bone marrow hematopoietic stem and progenitor cells from wildtype into Hem1 knockout mice increased bone resorption and normalized bone mass. These findings indicate that Hem1 plays a pivotal role in the maintenance of normal bone mass.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC9867982 | PMC |
| http://dx.doi.org/10.1016/j.jbc.2022.102841 | DOI Listing |
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