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To determine whether transplanted amniotic membrane mesenchymal stem cells (AMSCs) ameliorated the premature senescent phenotype of  Bmi-1 -deficient mice, postnatal 2-day-old  Bmi-1   −/−   mice were injected intraperitoneally with the second-passage AMSCs from amniotic membranes of β-galactosidase (β-gal) transgenic mice or wild-type (WT) mice labeled with DiI. Three reinjections were given, once every seven days. Phenotypes of 5-week-old β-gal +  AMSC-transplanted or 6-week-old DiI +  AMSC-transplanted  Bmi-1   −/−   mice were compared with vehicle-transplanted  Bmi-1   −/−   and WT mice. Vehicle-transplanted  Bmi-1   −/−   mice displayed growth retardation and premature aging with decreased cell proliferation and increased cell apoptosis; a decreased ratio and dysmaturity of lymphocytic series; premature osteoporosis with reduced osteogenesis and increased adipogenesis; redox imbalance and DNA damage in multiple organs. Transplanted AMSCs carried Bmi-1 migrated into multiple organs, proliferated and differentiated into multiple tissue cells, promoted growth and delayed senescence in  Bmi-1   −/−   transplant recipients. The dysmaturity of lymphocytic series were ameliorated, premature osteoporosis were rescued by promoting osteogenesis and inhibiting adipogenesis, the oxidative stress and DNA damage in multiple organs were inhibited by the AMSC transplantation in  Bmi-1   −/−   mice. These findings indicate that AMSC transplantation ameliorated the premature senescent phenotype of  Bmi-1 -deficient mice and could be a novel therapy to delay aging and prevent aging-associated degenerative diseases.

Anti-aging Effect of Transplanted Amniotic Membrane Mesenchymal Stem Cells in a Premature Aging Model of Bmi-1 Deficiency