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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Autores principales:	Wenbo Zhao, Philip Wiedemann, Eva Maria Wölfel, Mona Neven, Stephanie Peters, Thomas Imhof, Manuel Koch, Björn Busse, Michael Amling, Thorsten Schinke, Timur Alexander Yorgan
Formato:	article
Lenguaje:	EN
Publicado:	MDPI AG 2021
Materias:	bone remodeling <i>Col22a1</i> osteoclasts osteoblasts Biology (General) QH301-705.5
Acceso en línea:	https://doaj.org/article/0d79051c535c449090d472db7128244f
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spelling	oai:doaj.org-article:0d79051c535c449090d472db7128244f2021-11-25T17:10:29ZDecreased Trabecular Bone Mass in <i>Col22a1</i>-Deficient Mice10.3390/cells101130202073-4409https://doaj.org/article/0d79051c535c449090d472db7128244f2021-11-01T00:00:00Zhttps://www.mdpi.com/2073-4409/10/11/3020https://doaj.org/toc/2073-4409The 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.Wenbo ZhaoPhilip WiedemannEva Maria WölfelMona NevenStephanie PetersThomas ImhofManuel KochBjörn BusseMichael AmlingThorsten SchinkeTimur Alexander YorganMDPI AGarticlebone remodeling<i>Col22a1</i>osteoclastsosteoblastsBiology (General)QH301-705.5ENCells, Vol 10, Iss 3020, p 3020 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	bone remodeling <i>Col22a1</i> osteoclasts osteoblasts Biology (General) QH301-705.5
spellingShingle	bone remodeling <i>Col22a1</i> osteoclasts osteoblasts Biology (General) QH301-705.5 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
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.
format	article
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
title	Decreased Trabecular Bone Mass in <i>Col22a1</i>-Deficient Mice
title_short	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_sort	decreased trabecular bone mass in <i>col22a1</i>-deficient mice
publisher	MDPI AG
publishDate	2021
url	https://doaj.org/article/0d79051c535c449090d472db7128244f
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Decreased Trabecular Bone Mass in <i>Col22a1</i>-Deficient Mice

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