Disease relevance of Mepe

• Transfer of Mepe deficiency onto the Phex-deficient Hyp mouse background failed to correct hypophosphatemia and aberrant serum 1,25(OH)(2)D(3) levels [1].
• During the healing of non-stabilized tibial fractures, which occurs through endochondral ossification, Mepe expression was first detected in fibroblast-like cells within the callus by 6 days postfracture [2].
• Mepe, the gene encoding a tumor-secreted protein in oncogenic hypophosphatemic osteomalacia, is expressed in bone [3].

High impact information on Mepe

• Matrix extracellular phosphoglycoprotein (Mepe) is a proposed candidate for phosphatonin [1].
• Mepe, like Phex, is expressed by fully differentiated osteoblasts and down-regulated by 1,25-(OH)2D3 [3].
• Mepe became externalized in osteocyte lacunae during this period [2].
• We compared the Mepe expression profile with that of alkaline phosphatase, a marker of bone mineralization [2].
• By 10 and 14 days postfracture (the hard callus phase of repair), Mepe was expressed within late hypertrophic chondrocytes and osteocytes in the regenerating tissues [2].

Biological context of Mepe

• Here, we used an immunohistochemical approach to study whether Mepe has a role in murine long bone development and regeneration [2].
• Thus, Mepe appears to play a role in both long bone regeneration and the latter stages of skeletogenesis [2].

Anatomical context of Mepe

• Our data showed that Mepe protein was produced by osteoblasts and osteocytes during skeletogenesis, as early as 2 days postnatal [2].

Other interactions of Mepe

• In the remodeling phase of repair, Mepe expression levels remained high while alkaline phosphatase activity decreased [2].

References