Decreased Trabecular Bone Mass in <i>Col22a1</i>-Deficient Mice
The bone matrix is constantly remodeled by the coordinated activities of bone-forming osteoblasts and bone-resorbing osteoclasts. Whereas type I collagen is the most abundant bone matrix protein, there are several other proteins present, some of them specifically produced by osteoblasts. In a genome...
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MDPI AG
2021-11-01
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| author | Wenbo Zhao Philip Wiedemann Eva Maria Wölfel Mona Neven Stephanie Peters Thomas Imhof Manuel Koch Björn Busse Michael Amling Thorsten Schinke Timur Alexander Yorgan |
| author_facet | Wenbo Zhao Philip Wiedemann Eva Maria Wölfel Mona Neven Stephanie Peters Thomas Imhof Manuel Koch Björn Busse Michael Amling Thorsten Schinke Timur Alexander Yorgan |
| author_sort | Wenbo Zhao |
| collection | DOAJ |
| description | The bone matrix is constantly remodeled by the coordinated activities of bone-forming osteoblasts and bone-resorbing osteoclasts. Whereas type I collagen is the most abundant bone matrix protein, there are several other proteins present, some of them specifically produced by osteoblasts. In a genome-wide expression screening for osteoblast differentiation markers we have previously identified two collagen-encoding genes with unknown function in bone remodeling. Here we show that one of them, <i>Col22a1</i>, is predominantly expressed in bone, cultured osteoblasts, but not in osteoclasts. Based on this specific expression pattern we generated a <i>Col22a1</i>-deficient mouse model, which was analyzed for skeletal defects by µCT, undecalcified histology and bone-specific histomorphometry. We observed that <i>Col22a1</i>-deficient mice display trabecular osteopenia, accompanied by significantly increased osteoclast numbers per bone surface. In contrast, cortical bone parameters, osteoblastogenesis or bone formation were unaffected by the absence of <i>Col22a1</i>. Likewise, primary osteoblasts from <i>Col22a1</i>-deficient mice did not display a cell-autonomous defect, and they did not show altered expression of Rankl or Opg, two key regulators of osteoclastogenesis. Taken together, we provide the first evidence for a physiological function of <i>Col22a1</i> in bone remodeling, although the molecular mechanisms explaining the indirect influence of <i>Col22a1</i> deficiency on osteoclasts remain to be identified. |
| first_indexed | 2024-03-10T05:37:00Z |
| format | Article |
| id | doaj.art-0d79051c535c449090d472db7128244f |
| institution | Directory Open Access Journal |
| issn | 2073-4409 |
| language | English |
| last_indexed | 2024-03-10T05:37:00Z |
| publishDate | 2021-11-01 |
| publisher | MDPI AG |
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| series | Cells |
| spelling | doaj.art-0d79051c535c449090d472db7128244f2023-11-22T22:50:09ZengMDPI AGCells2073-44092021-11-011011302010.3390/cells10113020Decreased Trabecular Bone Mass in <i>Col22a1</i>-Deficient MiceWenbo Zhao0Philip Wiedemann1Eva Maria Wölfel2Mona Neven3Stephanie Peters4Thomas Imhof5Manuel Koch6Björn Busse7Michael Amling8Thorsten Schinke9Timur Alexander Yorgan10Department of Osteology and Biomechanics, University Medical Center Hamburg-Eppendorf, 20246 Hamburg, GermanyDepartment of Osteology and Biomechanics, University Medical Center Hamburg-Eppendorf, 20246 Hamburg, GermanyDepartment of Osteology and Biomechanics, University Medical Center Hamburg-Eppendorf, 20246 Hamburg, GermanyDepartment of Osteology and Biomechanics, University Medical Center Hamburg-Eppendorf, 20246 Hamburg, GermanyDepartment of Osteology and Biomechanics, University Medical Center Hamburg-Eppendorf, 20246 Hamburg, GermanyCenter for Biochemistry, Medical Faculty, University of Cologne, 50923 Cologne, GermanyCenter for Biochemistry, Medical Faculty, University of Cologne, 50923 Cologne, GermanyDepartment of Osteology and Biomechanics, University Medical Center Hamburg-Eppendorf, 20246 Hamburg, GermanyDepartment of Osteology and Biomechanics, University Medical Center Hamburg-Eppendorf, 20246 Hamburg, GermanyDepartment of Osteology and Biomechanics, University Medical Center Hamburg-Eppendorf, 20246 Hamburg, GermanyDepartment of Osteology and Biomechanics, University Medical Center Hamburg-Eppendorf, 20246 Hamburg, GermanyThe bone matrix is constantly remodeled by the coordinated activities of bone-forming osteoblasts and bone-resorbing osteoclasts. Whereas type I collagen is the most abundant bone matrix protein, there are several other proteins present, some of them specifically produced by osteoblasts. In a genome-wide expression screening for osteoblast differentiation markers we have previously identified two collagen-encoding genes with unknown function in bone remodeling. Here we show that one of them, <i>Col22a1</i>, is predominantly expressed in bone, cultured osteoblasts, but not in osteoclasts. Based on this specific expression pattern we generated a <i>Col22a1</i>-deficient mouse model, which was analyzed for skeletal defects by µCT, undecalcified histology and bone-specific histomorphometry. We observed that <i>Col22a1</i>-deficient mice display trabecular osteopenia, accompanied by significantly increased osteoclast numbers per bone surface. In contrast, cortical bone parameters, osteoblastogenesis or bone formation were unaffected by the absence of <i>Col22a1</i>. Likewise, primary osteoblasts from <i>Col22a1</i>-deficient mice did not display a cell-autonomous defect, and they did not show altered expression of Rankl or Opg, two key regulators of osteoclastogenesis. Taken together, we provide the first evidence for a physiological function of <i>Col22a1</i> in bone remodeling, although the molecular mechanisms explaining the indirect influence of <i>Col22a1</i> deficiency on osteoclasts remain to be identified.https://www.mdpi.com/2073-4409/10/11/3020bone remodeling<i>Col22a1</i>osteoclastsosteoblasts |
| spellingShingle | Wenbo Zhao Philip Wiedemann Eva Maria Wölfel Mona Neven Stephanie Peters Thomas Imhof Manuel Koch Björn Busse Michael Amling Thorsten Schinke Timur Alexander Yorgan Decreased Trabecular Bone Mass in <i>Col22a1</i>-Deficient Mice Cells bone remodeling <i>Col22a1</i> osteoclasts osteoblasts |
| title | Decreased Trabecular Bone Mass in <i>Col22a1</i>-Deficient Mice |
| title_full | Decreased Trabecular Bone Mass in <i>Col22a1</i>-Deficient Mice |
| title_fullStr | Decreased Trabecular Bone Mass in <i>Col22a1</i>-Deficient Mice |
| title_full_unstemmed | Decreased Trabecular Bone Mass in <i>Col22a1</i>-Deficient Mice |
| title_short | Decreased Trabecular Bone Mass in <i>Col22a1</i>-Deficient Mice |
| title_sort | decreased trabecular bone mass in i col22a1 i deficient mice |
| topic | bone remodeling <i>Col22a1</i> osteoclasts osteoblasts |
| url | https://www.mdpi.com/2073-4409/10/11/3020 |
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