Regulation of body length and bone mass by Gpr126/Adgrg6.
basic_science · Level V
Where this comes from
- Record sourced from PubMed, PMID 32219165.
- Also identified by DOI 10.1126/sciadv.aaz0368 and PMC identifier 7083604.
- Licence recorded as CC BY-NC.
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Abstract
Adhesion G protein-coupled receptor G6 (Adgrg6; also named GPR126) single-nucleotide polymorphisms are associated with human height in multiple populations. However, whether and how GPR126 regulates body height is unknown. In this study, we found that mouse body length was specifically decreased in <i>Osx-Cre;Gpr126<sup>fl/fl</sup></i> mice. Deletion of <i>Gpr126</i> in osteoblasts resulted in a remarkable delay in osteoblast differentiation and mineralization during embryonic bone formation. Postnatal bone formation, bone mass, and bone strength were also significantly affected in <i>Gpr126</i> osteoblast deletion mice because of defects in osteoblast proliferation, differentiation, and ossification. Furthermore, type IV collagen functioned as an activating ligand of <i>Gpr126</i> to regulate osteoblast differentiation and function by stimulating cAMP signaling. Moreover,the cAMP activator PTH(1-34), could partially restore the inhibition of osteoblast differentiation and the body length phenotype induced by <i>Gpr126</i> deletion.Together, our results demonstrated that COLIV-Gpr126 regulated body length and bone mass through cAMP-CREB signaling pathway.
Medical subject headings
- Body Height
- Bone and Bones
- Genetic Association Studies
- Receptors, G-Protein-Coupled
- Skeleton