ECTS Abstracts (2015) 1 P154

Wnt11 deficiency and osteoblast differentiation

Riina Rytivaara1,5, Irina Nagy2,6, Hanna Kokkonen1,5, Jorma Määttä3, Antti Koskela1,5, Juha Risteli4,5, Seppo Vainio2,6 & Juha Tuukkanen1,5


1Department of Anatomy and Cell Biology, University of Oulu, Oulu, Finland; 2Department of Medical Biochemistry, Oulu, Finland; 3Turku Center for Disease Modeling, University of Turku, Turku, Finland; 4Institute of Diagnostics, University of Oulu, Oulu, Finland; 5MRC Oulu, Oulu, Finland; 6Biocenter Oulu, Oulu, Finland.


Wnt-11 signalling uses mainly non-canonical pathways, but it is known to regulate bone formation, possibly through a β-catenin dependent pathway. Here we tested the role of Wnt-11 signalling in bone both in vivo and in vitro. Wnt11 knock-out (KO) mice and their wild type (WT) littermates were compared from two to ten months of age. Long bone histology, microcomputer tomography (μCT) and biomechanics were used. Bone marrow derived mesenchymal stem cells were isolated from Wnt11 knock-out and wild type mice and cultured for 14 days in osteogenic medium. Wnt11 gene expression was demonstrated with RT-PCR. Procollagen type 1 N-terminal propeptide (P1NP) production and mineralised nodule formation were analysed. RT-PCR showed that Wnt11 is expressed in mouse osteoblasts at days 3, 7, 9 and 14. Osteoblasts from KO animals proliferated and spread well and attached with numerous focal adhesions on day 14, but the differentiation and mineralisation revealed that Wnt11 deficiency retarded the osteogenic differentiation. The biomechanical tests and μCT did not show any difference between KO and WT. Wnt11 deficiency delays mouse osteoblast differentiation and mineralisation. So, Wnt-11 in bone seems not to be indispensable, since bone structure or biomechanical properties were normal in Wnt11 -deficient mice.

Disclosure: The authors declared no competing interests.

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