Tenascin-W inhibits proliferation and differentiation of preosteoblasts during endochondral bone formation
We identified a cDNA encoding mouse Tenascin-W (TN-W) upregulated by bone morphogenetic protein (Bmp)2 in ATDC5 osteo-chondroprogenitors. In adult mice, TN-W was markedly expressed in bone. In mouse embryos, during endochondral bone formation TN-W was localized in perichondrium/periosteum, but not i...
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| Published in: | Biochemical and biophysical research communications Vol. 356; no. 4; pp. 935 - 941 |
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| Main Authors: | , , , |
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| Language: | English |
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| Abstract | We identified a cDNA encoding mouse Tenascin-W (TN-W) upregulated by bone morphogenetic protein (Bmp)2 in ATDC5 osteo-chondroprogenitors. In adult mice,
TN-W was markedly expressed in bone. In mouse embryos, during endochondral bone formation
TN-W was localized in perichondrium/periosteum, but not in trabecular and cortical bones. During bone fracture repair, cells in the newly formed perichondrium/periosteum surrounding the cartilaginous callus expressed
TN-W. Furthermore,
TN-W was detectable in perichondrium/periosteum of
Runx2-null and
Osterix-null embryos, indicating that
TN-W is expressed in preosteoblasts. In CFU-F and -O cells, TN-W had no effect on initiation of osteogenesis of bone marrow cells, and in MC3T3-E1 osteoblastic cells TN-W inhibited cell proliferation and
Col1a1 expression. In addition, TN-W suppressed canonical Wnt signaling which stimulates osteoblastic differentiation. Our results indicate that
TN-W is a novel marker of preosteoblasts in early stage of osteogenesis, and that TN-W inhibits cell proliferation and differentiation of preosteoblasts mediated by canonical Wnt signaling. |
|---|---|
| AbstractList | We identified a cDNA encoding mouse Tenascin-W (TN-W) upregulated by bone morphogenetic protein (Bmp)2 in ATDC5 osteo-chondroprogenitors. In adult mice,
TN-W
was markedly expressed in bone. In mouse embryos, during endochondral bone formation
TN-W
was localized in perichondrium/periosteum, but not in trabecular and cortical bones. During bone fracture repair, cells in the newly formed perichondrium/periosteum surrounding the cartilaginous callus expressed
TN-W
. Furthermore,
TN-W
was detectable in perichondrium/periosteum of
Runx2
-null and
Osterix
null embryos, indicating that
TN-W
is expressed in preosteoblasts. In CFU-F and -O cells, TN-W had no effect on initiation of osteogenesis of bone marrow cells, and in MC3T3-E1 osteoblastic cells TN-W inhibited cell proliferation and
Col1a1
expression. In addition, TNW suppressed canonical Wnt signaling which stimulates osteoblastic differentiation. Our results indicate that
TN-W
is a novel marker of preosteoblasts in early stage of osteogenesis, and that TN-W inhibits cell proliferation and differentiation of preosteoblasts mediated by canonical Wnt signaling. We identified a cDNA encoding mouse Tenascin-W (TN-W) upregulated by bone morphogenetic protein (Bmp)2 in ATDC5 osteo-chondroprogenitors. In adult mice, TN-W was markedly expressed in bone. In mouse embryos, during endochondral bone formation TN-W was localized in perichondrium/periosteum, but not in trabecular and cortical bones. During bone fracture repair, cells in the newly formed perichondrium/periosteum surrounding the cartilaginous callus expressed TN-W. Furthermore, TN-W was detectable in perichondrium/periosteum of Runx2-null and Osterix-null embryos, indicating that TN-W is expressed in preosteoblasts. In CFU-F and -O cells, TN-W had no effect on initiation of osteogenesis of bone marrow cells, and in MC3T3-E1 osteoblastic cells TN-W inhibited cell proliferation and Col1a1 expression. In addition, TN-W suppressed canonical Wnt signaling which stimulates osteoblastic differentiation. Our results indicate that TN-W is a novel marker of preosteoblasts in early stage of osteogenesis, and that TN-W inhibits cell proliferation and differentiation of preosteoblasts mediated by canonical Wnt signaling. We identified a cDNA encoding mouse Tenascin-W (TN-W) upregulated by bone morphogenetic protein (Bmp)2 in ATDC5 osteo-chondroprogenitors. In adult mice, TN-W was markedly expressed in bone. In mouse embryos, during endochondral bone formation TN-W was localized in perichondrium/periosteum, but not in trabecular and cortical bones. During bone fracture repair, cells in the newly formed perichondrium/periosteum surrounding the cartilaginous callus expressed TN-W. Furthermore, TN-W was detectable in perichondrium/periosteum of Runx2-null and Osterix-null embryos, indicating that TN-W is expressed in preosteoblasts. In CFU-F and -O cells, TN-W had no effect on initiation of osteogenesis of bone marrow cells, and in MC3T3-E1 osteoblastic cells TN-W inhibited cell proliferation and Col1a1 expression. In addition, TN-W suppressed canonical Wnt signaling which stimulates osteoblastic differentiation. Our results indicate that TN-W is a novel marker of preosteoblasts in early stage of osteogenesis, and that TN-W inhibits cell proliferation and differentiation of preosteoblasts mediated by canonical Wnt signaling. |
| Author | Nakamura, Takashi Crombrugghe, Benoit de Akiyama, Haruhiko Kimura, Hiroaki |
| AuthorAffiliation | a Department of Orthopaedics, Kyoto University, Kyoto 606-8507, Japan b Department of Molecular Genetics, The University of Texas M. D. Anderson Cancer Center, Houston, TX 77030, USA |
| AuthorAffiliation_xml | – name: b Department of Molecular Genetics, The University of Texas M. D. Anderson Cancer Center, Houston, TX 77030, USA – name: a Department of Orthopaedics, Kyoto University, Kyoto 606-8507, Japan |
| Author_xml | – sequence: 1 givenname: Hiroaki surname: Kimura fullname: Kimura, Hiroaki organization: Department of Orthopaedics, Kyoto University, Kyoto 606-8507, Japan – sequence: 2 givenname: Haruhiko surname: Akiyama fullname: Akiyama, Haruhiko email: hakiyama@kuhp.kyoto-u.ac.jp organization: Department of Orthopaedics, Kyoto University, Kyoto 606-8507, Japan – sequence: 3 givenname: Takashi surname: Nakamura fullname: Nakamura, Takashi organization: Department of Orthopaedics, Kyoto University, Kyoto 606-8507, Japan – sequence: 4 givenname: Benoit de surname: Crombrugghe fullname: Crombrugghe, Benoit de organization: Department of Molecular Genetics, The University of Texas, M.D. Anderson Cancer Center, Houston, TX 77030, USA |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/17395156$$D View this record in MEDLINE/PubMed https://www.osti.gov/biblio/20991344$$D View this record in Osti.gov |
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| Snippet | We identified a cDNA encoding mouse Tenascin-W (TN-W) upregulated by bone morphogenetic protein (Bmp)2 in ATDC5 osteo-chondroprogenitors. In adult mice,
TN-W... We identified a cDNA encoding mouse Tenascin-W (TN-W) upregulated by bone morphogenetic protein (Bmp)2 in ATDC5 osteo-chondroprogenitors. In adult mice, TN-W... |
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| SubjectTerms | 60 APPLIED LIFE SCIENCES ADULTS Animals Bmp Bone Development - drug effects Bone Development - physiology BONE FRACTURES BONE MARROW CELLS BONE TISSUES BORON PHOSPHIDES Cell Differentiation - physiology CELL PROLIFERATION Embryonic Stem Cells - cytology Embryonic Stem Cells - physiology EMBRYOS MICE Mice, Inbred ICR Osteoblasts - cytology Osteoblasts - physiology Osteogenesis Osteogenesis - physiology Preosteoblast PROTEINS SKELETON Tenascin - metabolism Tenascin-W Wnt Proteins - metabolism Zebrafish Proteins - metabolism |
| Title | Tenascin-W inhibits proliferation and differentiation of preosteoblasts during endochondral bone formation |
| URI | https://dx.doi.org/10.1016/j.bbrc.2007.03.071 https://www.ncbi.nlm.nih.gov/pubmed/17395156 https://search.proquest.com/docview/20268468 https://search.proquest.com/docview/70373857 https://www.osti.gov/biblio/20991344 https://pubmed.ncbi.nlm.nih.gov/PMC3836430 |
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