eprintid: 10204558
rev_number: 9
eprint_status: archive
userid: 699
dir: disk0/10/20/45/58
datestamp: 2025-02-11 10:21:29
lastmod: 2025-02-11 10:21:29
status_changed: 2025-02-11 10:21:29
type: article
metadata_visibility: show
sword_depositor: 699
creators_name: Corcelli, Michelangelo
creators_name: Sagar, Rachel
creators_name: Petzendorfer, Ellen
creators_name: Hasan, Mohammad Mehedi
creators_name: van Dijk, Fleur S
creators_name: David, Anna L
creators_name: Guillot, Pascale V
title: Pleiotropic effects of a recessive Col1a2 mutation occurring in a mouse model of severe osteogenesis imperfecta
ispublished: pub
divisions: UCL
divisions: B02
divisions: D11
divisions: G12
keywords: Osteoblasts, Osteogenesis imperfecta, Bone and mineral metabolism, Collagens, Bone fracture, Osteoblast differentiation, Bone imaging, Bone density
note: Copyright: © 2025 Corcelli et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. http://creativecommons.org/licenses/by/4.0/
abstract: In Europe, approximately 85–90% of individuals with Osteogenesis Imperfecta (OI) have dominant pathogenic variants in the Col1a1 or Col1a2 genes whilst for Asian, especially Indian and Chinese cohorts, this ratio is much lower. This leads to decreased or abnormal Collagen type I production. Subsequently, bone formation is strongly reduced, causing bone fragility and liability to fractures throughout life. OI is clinically heterogeneous, with the severity ranging from mild to lethal depending on the gene and the type and location of the OI-causative variant and the subsequent effect on (pro) collagen type I synthesis. However, the specific effects on the phenotype and function of osteoblasts are not fully understood. To investigate this, one of the OI murine models was used, i.e. the oim/oim (OIM) mice, which closest resembling severely deforming OI in humans. We showed that in OIM, the Col1a2 mutation results in a multifactorial inhibition of the osteogenic differentiation and maturation as well as inhibition of osteoclastogenesis. The phenotype of differentiated OIM osteoblasts also differs from that of wild type mature osteoblasts, with upregulated oxidative cell stress and autophagy pathways. The extracellular accumulation of defective type I collagen fibres contributes to activation of the TGF-β signalling pathway and activates the inflammatory pathway. These effects combine to destabilise the balance of bone turnover, increasing bone fragility. Together, these findings identify the complex mechanisms underlying OI bone fragility in the OIM model of severe OI and can potentially enable identification of clinically relevant endpoints to assess the efficacy of innovative pro-osteogenic treatment for patients with OI.
date: 2025-02-05
date_type: published
publisher: Public Library of Science (PLoS)
official_url: https://doi.org/10.1371/journal.pone.0309801
oa_status: green
full_text_type: pub
language: eng
primo: open
primo_central: open_green
verified: verified_manual
elements_id: 2358865
doi: 10.1371/journal.pone.0309801
medium: Electronic-eCollection
pii: PONE-D-24-09480
lyricists_name: David, Anna
lyricists_name: Guillot, Pascale
lyricists_name: Petzendorfer, Ellen
lyricists_id: ADAVI52
lyricists_id: PVGUI46
lyricists_id: EPETZ05
actors_name: Guillot, Pascale
actors_id: PVGUI46
actors_role: owner
funding_acknowledgements: PVG received funding from the United Kingdom Medical Research Council (https://www.ukri.org/councils/mrc/) award 179068) and The Rosetrees Trust (https://rosetrees.org.uk/) award CM935. The sponsors did not play any role in the study design, data collection and analysis, decision to publish, or preparation of the manuscript.
full_text_status: public
publication: PLoS One
volume: 20
number: 2
article_number: e0309801
event_location: United States
issn: 1932-6203
editors_name: van Wijnen, Andre
citation:        Corcelli, Michelangelo;    Sagar, Rachel;    Petzendorfer, Ellen;    Hasan, Mohammad Mehedi;    van Dijk, Fleur S;    David, Anna L;    Guillot, Pascale V;      (2025)    Pleiotropic effects of a recessive Col1a2 mutation occurring in a mouse model of severe osteogenesis imperfecta.                   PLoS One , 20  (2)    , Article e0309801.  10.1371/journal.pone.0309801 <https://doi.org/10.1371/journal.pone.0309801>.       Green open access   
 
document_url: https://discovery.ucl.ac.uk/id/eprint/10204558/1/Guillot_Pleiotropic%20effects%20of%20a%20recessive%20Col1a2-journal.pone.0309801.pdf