ArticleThe American journal of pathology2004
Chicken collagen X regulatory sequences restrict transgene expression to hypertrophic cartilage in mice.
Article in The American journal of pathology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 20 citations in OpenAlex.
- Advances in Molecular Function and Recombinant Expression of Human Collagen.Pharmaceuticals (Basel, Switzerland) · 2025Review
- How to build an inducible cartilage-specific transgenic mouse.Arthritis research & therapy · 2014Review
- Defective endochondral ossification-derived matrix and bone cells alter the lymphopoietic niche in collagen X mouse models.Stem cells and development · 2013Article
- FoxA family members are crucial regulators of the hypertrophic chondrocyte differentiation program.Developmental cell · 2012Article
- Congenic mice confirm that collagen X is required for proper hematopoietic development.PloS one · 2010Article
- Altered endochondral ossification in collagen X mouse models leads to impaired immune responses.Developmental dynamics : an official publication of the American Association of Anatomists · 2008Article
- Heparan sulfate proteoglycans: a GAGgle of skeletal-hematopoietic regulators.Developmental dynamics : an official publication of the American Association of Anatomists · 2008Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Collagen X is produced by hypertrophic cartilage undergoing endochondral ossification. Transgenic mice expressing defective collagen X under the control of 4.7- or 1.6-kb chicken collagen X regulatory sequences yielded skeleto-hematopoietic defects (Jacenko O, LuValle P, Olsen BR: Spondylometaphyseal dysplasia in mice carrying a dominant-negative mutation in a matrix protein specific for cartilage-to-bone transition. Nature 1993, 365:56-61; Jacenko O, Chan D, Franklin A, Ito S, Underhill CB, Bateman JF, Campbell MR: A dominant interference collagen X mutation disrupts hypertrophic chondrocyte pericellular matrix and glycosaminoglycan and proteoglycan distribution in transgenic mice. Am J Pathol 2001, 159:2257-2269; Jacenko O, Roberts DW, Campbell MR, McManus PM, Gress CJ, Tao Z: Linking hematopoiesis to endochondral ossification through analysis of mice transgenic for collagen X. Am J Pathol 2002, 160:2019-2034). Current data indicate that the hematopoietic abnormalities do not result from extraskeletal expression of endogenous collagen X or the transgene. Organs from mice carrying either promoter were screened by immunohistochemistry, in situ hybridization, and Northern blot; transgene and mouse collagen X proteins and messages were detected only in hypertrophic cartilage. Likewise, reverse transcriptase-polymerase chain reaction revealed both transgene and mouse collagen X amplicons only in the endochondral skeleton of mice with the 4.7-kb promoter; however, in mice with the 1.6-kb promoter, multiple organs were transgene-positive. Collagen X and transgene amplicons were also detected in marrow, but likely resulted from contaminating trabecular bone; this was supported by reverse transcriptase-polymerase chain reaction analysis of rat tibial zones free of trabeculae. Our data demonstrate that in mice, the 4.7-kb chicken collagen X promoter restricts transcription temporo-spatially to that of endogenous collagen X, and imply that murine skeleto-hematopoietic defects result from transgene co-expression with collagen X. Moreover, the 4.7-kb hypertrophic cartilage-specific promoter could be used for targeting transgenes to this tissue site in mice.
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