Blood-induced bone loss in murine hemophilic arthropathy is prevented by blocking the iRhom2/ADAM17/TNF-α pathway

Author:

Haxaire Coline12,Hakobyan Narine3,Pannellini Tania4,Carballo Camila5,McIlwain David6,Mak Tak W.7,Rodeo Scott5,Acharya Suchitra8,Li Daniel1,Szymonifka Jackie2,Song Xiangqian3,Monette Sébastien9,Srivastava Alok10,Salmon Jane E.211,Blobel Carl P.17111213ORCID

Affiliation:

1. Arthritis and Tissue Degeneration Program and

2. Autoimmunity and Inflammation Program, Hospital for Special Surgery, New York, NY;

3. Pediatric Hematology/Oncology, Rush University Medical Center, Chicago, IL;

4. Department of Pathology and

5. Orthopedic Soft Tissue Research Program, Hospital for Special Surgery, New York, NY;

6. Baxter Laboratory in Stem Cell Biology, Department of Microbiology and Immunology, Stanford University, Stanford, CA;

7. Campbell Family Institute for Breast Cancer Research, Princess Margaret Cancer Center, University Health Network, Toronto, ON, Canada;

8. Pediatric Hematology/Oncology, Northwell Health, New Hyde Park, NY;

9. Laboratory of Comparative Pathology, Memorial Sloan Kettering Cancer Center, The Rockefeller University, Weill Cornell Medicine, New York, NY;

10. Department of Hematology, Christian Medical College, Vellore, India;

11. Department of Medicine and

12. Department of Biophysics, Physiology, and Systems Biology, Weill Cornell Medicine, New York, NY; and

13. Institute for Advanced Studies, Technical University Munich, Garching, Germany

Abstract

Key Points Blood and its components activated the iRhom2/ADAM17-dependent release of the proinflammatory cytokine TNF-α from macrophages. The iRhom2/ADAM17/TNF-α pathway emerged as a potential new target to prevent bone resorption following a joint bleed in mice.

Publisher

American Society of Hematology

Subject

Cell Biology,Hematology,Immunology,Biochemistry

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