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Msx1 role in craniofacial bone morphogenesis.

Ali Nassif1, Ibtisam Senussi1, Fleur Meary1

  • 1Cordeliers Research Center, INSERM UMRS 1138, Laboratory of Molecular Oral Pathophysiology, 15 rue de l'école de médecine, Paris, F-75006, France; Paris-Descartes University, Paris, F-75006, France; Pierre and Marie Curie University, Paris, F-75006, France; Paris-Diderot University, UFR Odontology, Paris, F-75006, France.

Bone
|June 15, 2014
PubMed
Summary
This summary is machine-generated.

The homeobox gene Msx1 influences bone development. Transgenic mice with increased Msx1 expression showed altered skull shape and bone matrix, but reduced mineralization, impacting osteoblast differentiation.

Keywords:
Animal modelBoneCollagenMineralizationMsx1Osteoblast

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Area of Science:

  • Skeletal Biology
  • Developmental Biology
  • Genetics

Background:

  • The homeobox gene Msx1 is crucial for embryonic and postnatal bone development.
  • Msx1 mutations in humans are linked to cleft palate and tooth agenesis.
  • Msx1's role in osteoblast differentiation and bone mineralization in vivo requires further investigation.

Purpose of the Study:

  • To investigate the in vivo function of Msx1 in bone development and shape.
  • To explore Msx1's role in osteoblast differentiation and bone mineralization.
  • To analyze subtle variations in bone shape using transgenic models.

Main Methods:

  • Generation of transgenic mice (Msx1-Tg) expressing Msx1 under the control of the mouse 2.3kb collagen 1 alpha 1 (Col1α1) promoter.
  • Analysis of skull and mandible morphology, bone matrix deposition, osteoblast parameters (number, proliferation, apoptosis), and bone mineralization (Von Kossa staining, μCT).

Main Results:

  • Msx1-Tg mice exhibited altered skull shape and increased bone matrix in mandibles compared to controls.
  • Increased osteoblast number, proliferation, and apoptosis were observed in Msx1-Tg mice.
  • Despite increased bone matrix, Msx1-Tg mice showed reduced bone mineralization due to altered osteoblastic differentiation.

Conclusions:

  • Msx1 acts as a bone modeling factor, particularly in membranous bone.
  • Msx1 stimulates trabecular bone metabolism but inhibits cortical bone growth via apoptosis.
  • Msx1 plays a role in regulating collagen-based bone mineralization.