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Interleukin‐1 Is Overexpressed in Injured Muscles Following Spinal Cord Injury and Promotes Neurogenic Heterotopic Ossification
Journal of bone and mineral research, 2022-03, Vol.37 (3), p.531-546
Tseng, Hsu‐Wen
Kulina, Irina
Girard, Dorothée
Gueguen, Jules
Vaquette, Cedryck
Salga, Marjorie
Fleming, Whitney
Jose, Beulah
Millard, Susan M
Pettit, Allison R
Schroder, Kate
Thomas, Gethin
Wheeler, Lawrie
Genêt, François
Banzet, Sébastien
Alexander, Kylie A
Lévesque, Jean‐Pierre
2022
Details
Autor(en) / Beteiligte
Tseng, Hsu‐Wen
Kulina, Irina
Girard, Dorothée
Gueguen, Jules
Vaquette, Cedryck
Salga, Marjorie
Fleming, Whitney
Jose, Beulah
Millard, Susan M
Pettit, Allison R
Schroder, Kate
Thomas, Gethin
Wheeler, Lawrie
Genêt, François
Banzet, Sébastien
Alexander, Kylie A
Lévesque, Jean‐Pierre
Titel
Interleukin‐1 Is Overexpressed in Injured Muscles Following Spinal Cord Injury and Promotes Neurogenic Heterotopic Ossification
Ist Teil von
Journal of bone and mineral research, 2022-03, Vol.37 (3), p.531-546
Ort / Verlag
Hoboken, USA: John Wiley & Sons, Inc
Erscheinungsjahr
2022
Link zum Volltext
Quelle
Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals
Beschreibungen/Notizen
ABSTRACT Neurogenic heterotopic ossifications (NHOs) form in periarticular muscles after severe spinal cord (SCI) and traumatic brain injuries. The pathogenesis of NHO is poorly understood with no effective preventive treatment. The only curative treatment remains surgical resection of pathological NHOs. In a mouse model of SCI‐induced NHO that involves a transection of the spinal cord combined with a muscle injury, a differential gene expression analysis revealed that genes involved in inflammation such as interleukin‐1β (IL‐1β) were overexpressed in muscles developing NHO. Using mice knocked‐out for the gene encoding IL‐1 receptor (IL1R1) and neutralizing antibodies for IL‐1α and IL‐1β, we show that IL‐1 signaling contributes to NHO development after SCI in mice. Interestingly, other proteins involved in inflammation that were also overexpressed in muscles developing NHO, such as colony‐stimulating factor‐1, tumor necrosis factor, or C‐C chemokine ligand‐2, did not promote NHO development. Finally, using NHO biopsies from SCI and TBI patients, we show that IL‐1β is expressed by CD68+ macrophages. IL‐1α and IL‐1β produced by activated human monocytes promote calcium mineralization and RUNX2 expression in fibro‐adipogenic progenitors isolated from muscles surrounding NHOs. Altogether, these data suggest that interleukin‐1 promotes NHO development in both humans and mice. © 2021 American Society for Bone and Mineral Research (ASBMR).
Sprache
Englisch
Identifikatoren
ISSN: 0884-0431
eISSN: 1523-4681
DOI: 10.1002/jbmr.4482
Titel-ID: cdi_hal_primary_oai_HAL_hal_04414260v1
Format
–
Schlagworte
Animals
,
Biopsy
,
Cbfa-1 protein
,
Chemokines
,
CYTOKINES
,
DISEASES AND DISORDERS OF/RELATED TO BONE (OTHER)
,
Gene expression
,
Humans
,
Inflammation
,
Inflammation - complications
,
Interleukin 1
,
Interleukin-1beta - metabolism
,
Life Sciences
,
Macrophages
,
Mice
,
Mineralization
,
Monocytes
,
Muscles
,
Muscles - pathology
,
Ossification (ectopic)
,
Ossification, Heterotopic - pathology
,
OSTEOIMMUNOLOGY
,
Spinal cord
,
Spinal Cord - metabolism
,
Spinal Cord - pathology
,
Spinal cord injuries
,
Spinal Cord Injuries - complications
,
Traumatic brain injury
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