Literature DB >> 18433297

Bone formation during distraction osteogenesis is dependent on both VEGFR1 and VEGFR2 signaling.

Kimberly A Jacobsen1, Zainab S Al-Aql, Chao Wan, Jennifer L Fitch, Stephanie N Stapleton, Zachary D Mason, Robert M Cole, Shawn R Gilbert, Thomas L Clemens, Elise F Morgan, Thomas A Einhorn, Louis C Gerstenfeld.   

Abstract

INTRODUCTION: Distraction osteogenesis (DO) is characterized by the induction of highly vascularized new bone formation through an intramembranous process largely devoid of the formation of cartilage.
MATERIALS AND METHODS: To test the hypothesis that DO is strictly dependent on vascualrization, we inhibited vascular endothelial growth factor (VEGF) activity by antibody blockade of both receptors VEGFR1 (Flt-1) and VEGFR2 (Flk-1) or only VEGFR2 (Flk-1) in a previously developed murine tibia DO model. During normal DO, VEGFR1 (Flt-1), VEGFR2 (Flk-1), VEGFR3 (Flt4) and all four VEGF ligand (A, B, C, and D) mRNAs are induced.
RESULTS: The expression of mRNA for the receptors generally paralleled those of the ligands during the period of active distraction. Bone formation, as assessed by muCT, showed a significant decrease with the double antibody treatment and a smaller decrease with single antibody treatment. Vessel volume, number, and connectivity showed progressive and significant inhibition in all of these of parameters between the single and double antibody blockade. Molecular analysis showed significant inhibition in skeletal cell development with the single and double antibody blockade of both VEGFR1 and 2. Interestingly, the single antibody treatment led to selective early development of chondrogenesis, whereas the double antibody treatment led to a failure of both osteogenesis and chondrogenesis.
CONCLUSIONS: Both VEGFR1 and VEGFR2 are functionally essential in blood vessel and bone formation during DO and are needed to promote osteogenic over chondrogenic lineage progression.

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Year:  2008        PMID: 18433297      PMCID: PMC2674537          DOI: 10.1359/jbmr.080103

Source DB:  PubMed          Journal:  J Bone Miner Res        ISSN: 0884-0431            Impact factor:   6.741


  48 in total

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Review 7.  Biological perspectives of delayed fracture healing.

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