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Spinal cord injury reprograms muscle fibroadipogenic progenitors to form heterotopic bones within muscles

Bone research 2022年第2期10卷 310-325页

作者： Hsu-Wen Tseng Dorothée Girard Kylie A.Alexander Susan M.Millard Frédéric Torossian Adrienne Anginot Whitney Fleming Jules Gueguen Marie-Emmanuelle Goriot Denis Clay Beulah Jose Bianca Nowlan allison r.pettit Marjorie Salga François Genêt Marie-Caroline Le Bousse-Kerdilès Sébastien Banzet Jean-Pierre Lévesque Mater research Institute-The University of Queensland WoolloongabbaQLDAustralia Institut de recherche Biomédicale des Armées(IrBA) INSERM UMRS-MD1197 ClamartFrance INSErM UMrS-MD 1197 Universitéde Paris-SaclayHôpital Paul BrousseVillejuifFrance INSErM UMS-44 Universitéde Paris-SaclayHôpital Paul BrousseVillejuifFrance UPOH(UnitéPéri Opératoire du Handicap Perioperative Disability Unit)Physical and Rehabilitation Medicine departmentRaymond-PoincaréHospitalAssistance Publique-Hôpitaux de Paris(AP-HP)GarchesFrance Universitéde Versailles Saint Quentin en Yvelines UFR Simone Veil-SantéEND:ICAP INSERM U1179Montigny le BretonneuxFrance

The cells of origin of neurogenic heterotopic ossifications(NHOs), which develop frequently in the periarticular muscles following spinal cord injuries(SCIs) and traumatic brain injuries, remain unclear because skeletal muscle harbors two progenitor cell populations: satellite cells(SCs), which are myogenic, and fibroadipogenic progenitors(FAPs), which are mesenchymal. Lineage-tracing experiments using the Cre recombinase/Lox P system were performed in two mouse strains with the fluorescent protein Zs Green specifically expressed in either SCs or FAPs in skeletal muscles under the control of the Pax7 or Prrx1 gene promoter, respectively. These experiments demonstrate that following muscle injury, SCI causes the upregulation of PDGFrα expression on FAPs but not SCs and the failure of SCs to regenerate myofibers in the injured muscle, with reduced apoptosis and continued proliferation of muscle resident FAPs enabling their osteogenic differentiation into NHOs. No cells expressing Zs Green under the Prrx1 promoter were detected in the blood after injury, suggesting that the cells of origin of NHOs are locally derived from the injured muscle. We validated these findings using human NHO biopsies. PDGFrα+mesenchymal cells isolated from the muscle surrounding NHO biopsies could develop ectopic human bones when transplanted into immunocompromised mice, whereas CD56+myogenic cells had a much lower potential. Therefore, NHO is a pathology of the injured muscle in which SCI reprograms FAPs to undergo uncontrolled proliferation and differentiation into osteoblasts.

关键词： progenitor injuries muscles

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Induction of osteoblast apoptosis stimulates macrophage efferocytosis and paradoxical bone formation

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Bone research 2024年第3期12卷 634-647页

作者： Lena Batoon Amy Jean Koh Susan Marie Millard Jobanpreet Grewal Fang Ming Choo rahasudha Kannan Aysia Kinnaird Megan Avey Tatyana Teslya allison robyn pettit Laurie K.McCauley Hernan roca Department of Periodontics and Oral Medicine University of MichiganSchool of DentistryAnn ArborMI 48109USA Mater research Institute The University of QueenslandBrisbaneQLD 4102Australia Department of Pathology University of MichiganMedical SchoolAnn ArborMI 48109USA

Apoptosis is crucial for tissue homeostasis and organ *** bone,apoptosis is recognized to be a main fate of osteoblasts,yet the relevance of this process remains *** our murine model with inducible Caspase 9,the enzyme that initiates intrinsic apoptosis,we triggered apoptosis in a proportion of mature osteocalcin(OCN^(+))osteoblasts and investigated the impact on postnatal bone development.

关键词： development homeostasis bone

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