Postnatal Runx2 deletion leads to low bone mass and adipocyte accumulation in mice bone tissues

Biochem Biophys Res Commun. 2019 Sep 3;516(4):1229-1233. doi: 10.1016/j.bbrc.2019.07.014. Epub 2019 Jul 9.

Abstract

Global gene deletion studies have established that Runt-related transcription factor-2 (Runx2) is essential during skeletogenesis for osteoblastic differentiation in both intramembranous and endochondral ossification processes. However, the postnatal significance of Runx2 in vivo is poorly understood because a global Runx2 deletion causes perinatal lethality. In this study, we generated tamoxifen-induced Runx2 global deficient mice by crossing Runx2flox mice with ROSA26-CreERT2 mice (Rosa26-CreERT2; Runx2flox/flox). Four-week-old mice were intraperitoneally treated with tamoxifen for five consecutive days, sacrificed, and analyzed six weeks after tamoxifen administration. Deletion of Runx2 led to low bone mass, which is associated with decreased bone formation and bone resorption as well as excessive bone marrow adiposity. Collectively, postnatal Runx2 absolutely plays an important role in maintaining the homeostasis of bone tissues not only in bone mass, but also in the bone marrow environment.

Keywords: Aging; Bone marrow adiposity; Conditional knockout; Osteoporosis; Runx2.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adipocytes / cytology*
  • Adiposity
  • Aging
  • Animals
  • Bone Density*
  • Bone Marrow Cells / cytology
  • Core Binding Factor Alpha 1 Subunit / genetics*
  • Core Binding Factor Alpha 1 Subunit / physiology*
  • Crosses, Genetic
  • Disease Models, Animal
  • Female
  • Gene Deletion*
  • Genotype
  • Male
  • Mice
  • Mice, Transgenic
  • Osteoporosis
  • Phenotype
  • Tamoxifen / pharmacology
  • Tibia
  • X-Ray Microtomography

Substances

  • Core Binding Factor Alpha 1 Subunit
  • Runx2 protein, mouse
  • Tamoxifen