Collagen XIII is a conserved transmembrane collagen with wide distribution in various tissues. It can be enzymatically cleaved to form a soluble bioactive molecule with relevance to cell proliferation, migration and adhesion. Collagen XIII overexpression in mice causes a massive bone overgrowth with no defects in early skeletal development. The bone phenotype of Col13a1OE mice is most apparent in long tubular bones but also present in calvariae. Our findings show that type XIII collagen is a significant regulator in the early osteoblast differentiation.
We have found major differences in proliferation rate, morphology and activity of primary osteoblasts derived from Col13a1OE mice compared to controls. We have also discovered qualitative changes in bones of Col13a1OE mice. Micro-computed tomography (μCT) and X-ray photoelectron spectroscopy (XPS) analyses of 25 week old Col13a1OE mouse femurs reveal tenfold increase in cortical bone volume whereas the calcium content is decreased by 51% compared to WT mice.
In summary, while collagen I is the main protein component of bones, our mouse models show that altered collagen XIII expression has striking effects on bone. Collagen XIII enhances the early steps of osteogenic differentiation and is an important regulator of bone remodeling and homeostasis.
17 May 2014 - 20 May 2014