title: Allogeneic Bone Marrow Transplant from MRL/MpJ Super-Healer Mice Does Not Improve Articular Cartilage Repair in the C57Bl/6 Strain.
abstract: BACKGROUND
  Articular cartilage has been the focus of multiple strategies to improve its regenerative/ repair capacity. The Murphy Roths Large (MRL/MpJ) "super-healer" mouse demonstrates an unusual enhanced regenerative capacity in many tissues and provides an opportunity to further study endogenous cartilage repair. The objective of this study was to test whether the super-healer phenotype could be transferred from MRL/MpJ to non-healer C57Bl/6 mice by allogeneic bone marrow transplant.
  
  
  METHODS
  The healing of 2mm ear punches and full thickness cartilage defects was measured 4 and 8 weeks after injury in control C57Bl/6 and MRL/MpJ "super-healer" mice, and in radiation chimeras reconstituted with bone marrow from the other mouse strain. Healing was assessed using ear hole diameter measurement, a 14 point histological scoring scale for the cartilage defect and an adapted version of the Osteoarthritis Research Society International scale for assessment of osteoarthritis in mouse knee joints.
  
  
  RESULTS
  Normal and chimeric MRL mice showed significantly better healing of articular cartilage and ear wounds along with less severe signs of osteoarthritis after cartilage injury than the control strain. Contrary to our hypothesis, however, bone marrow transplant from MRL mice did not confer improved healing on the C57Bl/6 chimeras, either in regards to ear wound healing or cartilage repair.
  
  
  CONCLUSIONS
  The elusive cellular basis for the MRL regenerative phenotype still requires additional study and may possibly be dependent on additional cell types external to the bone marrow.
authors.affiliation: McCaig Institute for Bone and Joint Health, Department of Surgery, University of Calgary, Calgary, Alberta, Canada.
authors.forename: Catherine A
authors.initials: CA
authors.lastname: Leonard
authors.affiliation: Calvin, Phoebe, and Joan Snyder Institute for Chronic Disease, Department of Physiology and Pharmacology, University of Calgary, Calgary, Alberta, Canada.
authors.forename: Woo-Yong
authors.initials: WY
authors.lastname: Lee
authors.affiliation: McCaig Institute for Bone and Joint Health, Department of Surgery, University of Calgary, Calgary, Alberta, Canada.
authors.forename: Pankaj
authors.initials: P
authors.lastname: Tailor
authors.affiliation: McCaig Institute for Bone and Joint Health, Department of Surgery, University of Calgary, Calgary, Alberta, Canada.
authors.forename: Paul T
authors.initials: PT
authors.lastname: Salo
authors.affiliation: Calvin, Phoebe, and Joan Snyder Institute for Chronic Disease, Department of Physiology and Pharmacology, University of Calgary, Calgary, Alberta, Canada.
authors.forename: Paul
authors.initials: P
authors.lastname: Kubes
authors.affiliation: McCaig Institute for Bone and Joint Health, Department of Surgery, University of Calgary, Calgary, Alberta, Canada.
authors.forename: Roman J
authors.initials: RJ
authors.lastname: Krawetz
mesh_terms: D000818:Animals; D015415:Biomarkers / Q000378:metabolism; D016026:Bone Marrow Transplantation; D002358:Cartilage, Articular / Q000473:pathology*; D002678:Chimera; D018450:Disease Progression; D004423:Ear / Q000473:pathology; D007719:Knee Joint / Q000473:pathology; D008815:Mice, Inbred Strains; D010003:Osteoarthritis / Q000473:pathology; D014184:Transplantation, Homologous; D014945:Wound Healing
chemical_list: D015415:Biomarkers