Objectives: To define the requirements for individual VEGF isoforms in tooth development, through analysis of mice that express single VEGF isoforms, VEGF120/120, VEGF164/164 and VEGF188/188 mice (Stalmans et al., 2002). Methods: Mouse litters obtained from crosses of heterozygous VEGF120, 164 or 188 isoform mice were obtained at E13.5 and E18.5. Mouse pups were fixed in IHC Zinc Fixative (BD Pharmingen), embedded in paraffin, and thin sectioned. Immunohistochemical analysis was performed using the purified rat anti-mouse CD34 monoclonal antibody (BD Pharmingen), and MOM Kit (Vector Laboratories, Burlingame, CA). Stained sections were analyzed using a Leica DMRE microscope and Zeiss Axiocam digital camera. Results: Our analyses revealed distinct vasculature defects in VEGF 120/120 mouse embryos characterized by reduced blood vessel formation. Surprisingly, despite the reduced vascularization of the jaw in VEGF120/120 mice at E 13.5 and E 18.5, tooth development appeared relatively normal. No obvious phenotype was observed in VEGF164/164 or VEGF188/188 isoform animals. Conclusions: These results suggest distinct roles for VEGF isforms in tooth vascularization. VEGF120 is inadequate to support normalization whereas VEGF isoform 164 or 188 is sufficient. Furthermore, we conclude that tooth development can occur in the absence of normal vascularization. Additional analyses, including examination of tooth eruption in later staged embryos are being conducted to identify potential subtle defects in VEGF isoform transgenic mice. Supported by grants CA45548 (PAD).

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