Display options
Cite
Li H, Lu A, Gao X, et al. Improved Bone Quality and Bone Healing of Dystrophic Mice by Parabiosis. Metabolites. 2021;11(4)doi: 10.3390/metabo11040247.
Li, H., Lu, A., Gao, X., Tang, Y., Ravuri, S., Wang, B., & Huard, J. (2021). Improved Bone Quality and Bone Healing of Dystrophic Mice by Parabiosis. Metabolites, 11(4), . https://doi.org/10.3390/metabo11040247
Li, Hongshuai, et al. "Improved Bone Quality and Bone Healing of Dystrophic Mice by Parabiosis." Metabolites vol. 11,4 (2021). doi: https://doi.org/10.3390/metabo11040247
Li H, Lu A, Gao X, Tang Y, Ravuri S, Wang B, Huard J. Improved Bone Quality and Bone Healing of Dystrophic Mice by Parabiosis. Metabolites. 2021 Apr 16;11(4). doi: 10.3390/metabo11040247. PMID: 33923553; PMCID: PMC8073674.
Copy Download .nbib Format: NLM
Share it on

Metabolites. 2021 Apr 16;11(4). doi: 10.3390/metabo11040247.

Improved Bone Quality and Bone Healing of Dystrophic Mice by Parabiosis.

Metabolites

Hongshuai Li, Aiping Lu, Xueqin Gao, Ying Tang, Sudheer Ravuri, Bing Wang, Johnny Huard

Affiliations

  1. Department of Orthopaedic Surgery, University of Pittsburgh, Pittsburgh, PA 15260, USA.
  2. Steadman Philippon Research Institute, Vail, CO 81657, USA.

PMID: 33923553 PMCID: PMC8073674 DOI: 10.3390/metabo11040247

Abstract

Duchenne muscular dystrophy (DMD) is a degenerative muscle disorder characterized by a lack of dystrophin expression in the sarcolemma of muscle fibers. DMD patients acquire bone abnormalities including osteopenia, fragility fractures, and scoliosis indicating a deficiency in skeletal homeostasis. The dKO (dystrophin/Utrophin double knockout) is a more severe mouse model of DMD than the mdx mouse (dystrophin deficient), and display numerous clinically-relevant manifestations, including a spectrum of degenerative changes outside skeletal muscle including bone, articular cartilage, and intervertebral discs. To examine the influence of systemic factors on the bone abnormalities and healing in DMD, parabiotic pairing between dKO mice and mdx mice was established. Notably, heterochronic parabiosis with young mdx mice significantly increased bone mass and improved bone micro-structure in old dKO-hetero mice, which showed progressive bone deterioration. Furthermore, heterochronic parabiosis with WT C56/10J mice significantly improved tibia bone defect healing in dKO-homo mice. These results suggest that systemic blood-borne factor(s) and/or progenitors from WT and young mdx mice can influence the bone deficiencies in dKO mice. Understanding these circulating factors or progenitor cells that are responsible to alleviate the bone abnormalities in dKO mice after heterochronic parabiosis might be useful for the management of poor bone health in DMD.

Keywords: Duchenne muscular dystrophy; bone abnormality/healing; circulating factors and progenitors; parabiosis

References

  1. Anat Rec. 1965 Feb;151:151-7 - PubMed
  2. Cell. 1997 Aug 22;90(4):717-27 - PubMed
  3. Osteoporos Int. 2003 Sep;14(9):761-7 - PubMed
  4. Circulation. 1978 Jun;57(6):1122-9 - PubMed
  5. J Bone Miner Res. 2011 Aug;26(8):1891-903 - PubMed
  6. J Cell Physiol. 2012 Feb;227(2):821-8 - PubMed
  7. Science. 2007 Aug 10;317(5839):807-10 - PubMed
  8. Int J Cardiol. 1990 Mar;26(3):271-7 - PubMed
  9. FASEB J. 2013 Sep;27(9):3619-31 - PubMed
  10. PLoS One. 2013 Jul 29;8(7):e69567 - PubMed
  11. Dev Med Child Neurol. 2002 Oct;44(10):695-8 - PubMed
  12. Cell. 1997 Aug 22;90(4):729-38 - PubMed
  13. Aging Cell. 2013 Jun;12(3):525-30 - PubMed
  14. Am J Physiol. 1959 Jan;196(1):110-2 - PubMed
  15. J Orthop Res. 2008 Feb;26(2):165-75 - PubMed
  16. Acta Neuropathol Commun. 2018 Apr 24;6(1):31 - PubMed
  17. Mol Ther. 2007 Jun;15(6):1086-92 - PubMed
  18. Proc Natl Acad Sci U S A. 1984 Feb;81(4):1189-92 - PubMed
  19. J Clin Invest. 2019 May 23;129(8):3214-3223 - PubMed
  20. Am J Physiol. 1960 Dec;199:1097-100 - PubMed
  21. J Pediatr Orthop. 2000 Jan-Feb;20(1):71-4 - PubMed
  22. Adv Healthc Mater. 2013 Sep;2(9):1277-84 - PubMed
  23. Cell. 1987 Dec 24;51(6):919-28 - PubMed
  24. J Cell Biol. 1997 Feb 24;136(4):883-94 - PubMed
  25. Hum Mol Genet. 2019 Sep 15;28(18):3101-3112 - PubMed
  26. Am J Physiol. 1964 Aug;207:449-51 - PubMed
  27. J Bone Miner Res. 2020 Apr;35(4):738-752 - PubMed
  28. Hum Mol Genet. 2019 May 15;28(10):1738-1751 - PubMed
  29. J Cell Biol. 2001 May 28;153(5):1133-40 - PubMed
  30. J Rehabil Med. 2001 Jul;33(4):150-5 - PubMed
  31. Biochem Biophys Res Commun. 2007 Mar 9;354(2):453-8 - PubMed
  32. Nature. 2005 Feb 17;433(7027):760-4 - PubMed
  33. J Biochem. 1995 Nov;118(5):959-64 - PubMed
  34. Genesis. 2010 Mar;48(3):171-82 - PubMed
  35. Science. 1987 Oct 16;238(4825):347-50 - PubMed
  36. Cell Immunol. 2005 Feb;233(2):133-9 - PubMed
  37. Cochrane Database Syst Rev. 2005 Jul 20;(3):CD003178 - PubMed
  38. Clin Orthop Relat Res. 1975 Jul-Aug;(110):293-301 - PubMed
  39. Muscle Nerve. 2018 Oct;58(4):573-582 - PubMed
  40. J Orthop Res. 2013 Mar;31(3):343-9 - PubMed
  41. Science. 1989 Jun 30;244(4912):1578-80 - PubMed
  42. Proc Soc Exp Biol Med. 1951 Apr;76(4):833-5 - PubMed

Publication Types

Grant support