Deletion of the mechanosensitive protein Piezo1 in Col2a1-expressing cells impairs postnatal trabecular bone formation

Introduction

Recently, we and others identified Piezo1 as the long-sought mechanosensor in osteocytes [1] [2] [3] [4]. Mice with an osteocyte-specific deletion (Dmp1-cre) of Piezo1 are osteoporotic and their long bones do not respond to mechanical stimulation [1]. Furthermore, osteoblast-specific deletion (Runx2-cre) led to an even more severe skeletal phenotype. Adult mice had no secondary spongiosa and rib fractures occurred in two-week-old mice. Most interestingly however, the deletion of Piezo1 in chondrocytes (Col2a1-cre) led to a similar phenotype as in mice with an osteoblast-specific deletion. We therefore examined the development of the skeletal phenotype in Piezo1 ^Col2a1cre mice starting from birth up to 12 weeks of age.

Publikationsverlauf

Artikel online veröffentlicht:
04. November 2021

• References

• 1 Hendrickx et al. J Bone Miner Res 2021; 36(2): 369–384.
• 2 Sun et al. Elife 2019; 8: e47454.
• 3 Li et al. Elife 2019; 8: e49631.
• 4 Wang et al. Nat Commun 2020; 11(1): 282