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Mesenchymal regulation of vascular invasion and matrix remodeling during intramembranous ossification
Author(s) -
Butcher Kristin D.,
Jheon Andrew H.,
Smith Francis J.,
Schneider Richard A.
Publication year - 2009
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.23.1_supplement.646.2
Subject(s) - mesenchyme , mesoderm , intramembranous ossification , quail , biology , ingression , mesenchymal stem cell , microbiology and biotechnology , osteoclast , ossification , anatomy , cartilage , embryonic stem cell , pathology , endocrinology , embryogenesis , in vitro , embryo , medicine , gene , genetics , gastrulation
With the goal of devising new treatments for skeletal disease and injury, there is much need to discover mechanisms through which mesenchyme makes bone. Many studies have pinpointed molecular factors that induce the osteogenic differentiation of mesenchyme in vitro, but given that a clinical objective is to engineer mesenchyme for applications in vivo, more work is required to identify critical interactions between osteogenic mesenchyme and surrounding tissues. We investigate the extent to which mesenchyme regulates vascular invasion and matrix remodeling. In the developing jaws and face, all bone comes from neural crest mesenchyme (NCM) whereas angioblasts and osteoclasts arise from mesoderm. We take advantage of these distinct embryonic origins and transplant faster developing quail NCM into slower developing duck embryos. Previously, using this quail‐duck chimeric system, we have shown that NCM makes bone by executing autonomous molecular and histogenic programs. Here, we assess the effects of NCM on host‐derived blood vessels and osteoclasts using gene expression, histology, and whole‐mount staining analyses. We find that quail donor‐NCM induces premature vascular invasion by the duck host during ossification but not at earlier stages. NCM also influences osteoclast activity. We conclude that NCM plays an important role in synchronizing the timing of vascular invasion and matrix remodeling.