Contribution of metabolic disease to bone fragility in MAGP1-deficient mice.

ABSTRACT: Microfibril-associated glycoprotein-1 (MAGP1) is an extracellular matrix protein that interacts with fibrillin and is involved in regulating the bioavailability of signaling molecules such as TGFβ. Mice with germline MAGP1 deficiency (Mfap2^-/-) develop increased adiposity, hyperglycemia, insulin resistance, bone marrow adipose tissue expansion, reduced cancellous bone mass, cortical bone thinning and bone fragility. The goal of this study was to assess whether the Mfap2^-/- bone phenotypes were due to loss of MAGP1 locally or secondary to a change in whole body physiology (metabolic dysfunction). To do this, mice with conditional deletion of MAGP1 in the limb skeleton were generated by crossing MAGP1-flox mice (Mfap2^lox/lox) with Prx1-Cre mice. Mfap2^Prx

SUBMITTER: Turecamo SE 

PROVIDER: S-EPMC6077988 | biostudies-literature | 2018 Apr

REPOSITORIES: biostudies-literature