ArticleScientific reports2025
A transgenic mouse line with a 58 kb fragment deletion shows skeletal defects.
Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
Abstract
Previously, a transgenic mouse line lacking a 58 kb fragment deletion including the upstream and exon1 of Fam20a gene (58 kb deletion mouse) was generated and showed growth retardation. The aim of this study was to characterize the skeletal phenotype of the homozygous 58 kb deletion mouse (58 kb-/-). Our results showed that body size and bone length of the 58 kb-/- mice were smaller than those of wild-type (WT) mice. The microcomputed tomography (µCT) analyses of trabecular and cortical bones in the 58 kb-/- displayed lower bone volume, thinner trabeculae and thinner bone cortex as compared to WT. Histological examination of the 58 kb-/- growth plate demonstrated disorganized chondrocyte zones and extended hypertrophic zone. The qPCR results showed downregulation of several osteoblast differentiation markers in the 58 kb-/- long bone. Immunohistochemical examination demonstrated reduced chondrocyte proliferation, apoptosis and increased collagen X expression in the 58 kb-/- growth plate. Our data showed a lower number of osteoblasts and osteoclasts in the 58 kb-/- as compared to WT. In vitro cell culture study demonstrated the 58 kb-/- showed a lower number of bone marrow stromal cells and osteoprogenitors. The extent of matrix mineralization was impaired in the 58 kb-/- osteoblast cultures. In conclusion, endochondral ossification defects and reduced number of osteoblasts and their precursors led to the bone phenotype in the 58 kb-/-, indicating that the genes deleted in this 58 kb likely play an important role in skeletal development.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.