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IGF-1 from bone marrow Adipoq-lineage cells stimulates endocortical bone formation in mature female mice
Joshua C Bertels1, Jasmin Koehnken Sawall1, Brian Dulmovits2
1Department of Surgery, Translational Research Program in Pediatric Orthopedics, The Children's Hospital of Philadelphia, Philadelphia, PA, 19104, United States.
Insulin-like growth factor 1 (IGF-1) is an anabolic signal promoting growth, differentiation and function of both embryonic and postnatal tissues. Both endocrine and paracrine functions of IGF-1 have been documented to regulate bone growth and BM hematopoiesis. Local production of IGF-1 from various cell types may contribute differently to the overall bioactivity of IGF-1 in bone, but relevant sources and mechanisms are yet to be fully elucidated. Here, we report that the Adipoq+ stromal cells are a notable source of IGF-1 in the BM of postnatal mice. Deletion of IGF-1 with Adipoq-Cre diminished endocortical bone formation and cortical bone mass in mature female mice. On the other hand, the trabecular bone parameters or hematopoietic properties were not affected in mutant mice of either sex. The study uncovers a local source of IGF-1 in the BM microenvironment that contributes to bone anabolic regulation in a site-specific manner.
Insulin-like growth factor 1 (IGF-1) is an anabolic signal promoting growth, differentiation and function of both embryonic and postnatal tissues. Both endocrine and paracrine functions of IGF-1 have been documented to regulate bone growth and BM hematopoiesis. Local production of IGF-1 from various cell types may contribute differently to the overall bioactivity of IGF-1 in bone, but relevant sources and mechanisms are yet to be fully elucidated. Here, we report that the Adipoq+ stromal cells are a notable source of IGF-1 in the BM of postnatal mice. Deletion of IGF-1 with Adipoq-Cre diminished endocortical bone formation and cortical bone mass in mature female mice. On the other hand, the trabecular bone parameters or hematopoietic properties were not affected in mutant mice of either sex. The study uncovers a local source of IGF-1 in the BM microenvironment that contributes to bone anabolic regulation in a site-specific manner.
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