MRL mice fail to heal the heart in response to ischemia‐reperfusion injury

@article{Abdullah2005MRLMF,
  title={MRL mice fail to heal the heart in response to ischemia‐reperfusion injury},
  author={Ibrahim Abdullah and John J. Lepore and Jonathan A. Epstein and Michael S. Parmacek and Peter J Gruber},
  journal={Wound Repair and Regeneration},
  year={2005},
  volume={13}
}
The MRL/MpJ mouse strain has been reported to recover after right ventricular cryoinjury without scar formation or evidence of ventricular dysfunction, suggesting that this mouse strain harbors genetic traits that confer the capacity for adult myocardium to regenerate. We therefore sought to assess the capacity of adult MRL myocardium to regenerate in a left ventricular ischemia‐reperfusion model of myocardial infarction, which more closely recapitulates injury that occurs in human disease. MRL… Expand
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References

SHOWING 1-10 OF 19 REFERENCES
Heart regeneration in adult MRL mice
TLDR
It is demonstrated that a severe transmural, cryogenically induced infarction of the right ventricle heals extensively within 60 days, with the restoration of normal myocardium and function. Expand
Scar formation after ischemic myocardial injury in MRL mice.
TLDR
The findings suggest that scarless recovery from myocardial injury is possible in mammalian ventricles, and if applicable to humans, these results could have significant clinical implications in the management of patients with myocardia infarction. Expand
Haematopoietic stem cells do not transdifferentiate into cardiac myocytes in myocardial infarcts
TLDR
Results indicate that haematopoietic stem cells do not readily acquire a cardiac phenotype, and raise a cautionary note for clinical studies of infarct repair. Expand
Varying susceptibility to myocardial infarction among C57BL/6 mice of different genetic background.
Genetically manipulated mouse lines are invaluable to investigate the effects of a single gene on sensitivity to ischemia. When choosing appropriate controls, we were concerned that intrinsic,Expand
Heart Regeneration in Zebrafish
TLDR
It is demonstrated histologically that zebrafish fully regenerate hearts within 2 months of 20% ventricular resection, showing that injury-induced cardiomyocyte proliferation in zebra fish can overcome scar formation, allowing cardiac muscle regeneration. Expand
Repair and reorganization of minced cardiac muscle in the adult newt (Notophthalmus viridescens)
TLDR
The results suggest that amphibian cardiac muscle has histogenetic and proliferative capacities not attributable to mammalian cardiac muscle. Expand
Aberrant wound healing and TGF-β production in the autoimmune-prone MRL/+ mouse
TLDR
The novel observations that, compared to normal controls, MRL/+ hematopoietic cells overproduce TGF-β1 and manifest impaired inflammatory responses to lipopolysaccharide challenge suggest that the aberrant wound healing phenotype of MRL mice is independent of their propensity to develop autoimmunity. Expand
Aberrant wound healing and TGF-beta production in the autoimmune-prone MRL/+ mouse.
TLDR
The novel observations that, compared to normal controls, MRL/+ hematopoietic cells overproduce TGF-beta1 and manifest impaired inflammatory responses to lipopolysaccharide challenge suggest that the aberrant wound healing phenotype of MRL mice is independent of their propensity to develop autoimmunity. Expand
Haematopoietic stem cells adopt mature haematopoietic fates in ischaemic myocardium
TLDR
The data suggest that even in the microenvironment of the injured heart, c-kit-enriched BM cells, Lin- c- Kit+ BM cells and c-Kit+ Thy1.1lo Lin- Sca-1+ long-term reconstituting haematopoietic stem cells adopt only traditional haem atopoetic fates. Expand
Cell cycle reentry of ventricular and atrial cardiomyocytes and cells within the epicardium following amputation of the ventricular apex in the axolotl, Amblystoma mexicanum: confocal microscopic immunofluorescent image analysis of bromodeoxyuridine-labeled nuclei
  • I. Flink
  • Biology, Medicine
  • Anatomy and Embryology
  • 2002
TLDR
Results suggest that renewed cell division is a specific response to wounding of the ventricle and release of a growth factor may be responsible for the specific localized mitotic ventricular cardiomyocyte response adjacent to the wound, and the more generalized atrial proliferative response distal to the amputation. Expand
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