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Our results demonstrate that hypoxia increases LRP1 expression through HIF-1α and that LRP1 overexpression mediates hypoxia-induced VLDL-CE uptake and accumulation in cardiomyocytes.

Background: Whether aging modifies mesenchymal stem cell (MSC) properties is unknown. Aim: To compare the differentiation capacity of human CD105 + MSCs obtained from young and elderly donors. Methods and results: Cells were obtained from young (n = 10, 24 T 6.4 years) and elderly (n = 9, 77 T 8.4 years) donors. Cell senescence was assessed by telomere length assays and lipofuscin accumulation. Cell pluripotentiality was analysed by adipogenic and osteogenic induction media, and myocyte phenotype was attempted with 5-azacytidine (5-AZ). Immunofluorescence, Western blot, transmission electron microscopy and fluo-4 confocal imaging were used to analyse the sarcomere, gap junctions and Ca 2+ dynamics. Cells obtained from young and elderly donors showed no significant differences in relative telomere length (40.1 T 6.4% and 40.3 T 3.6%, p = 0.9) and lipofuscin accumulation. Adipogenic and osteogenic potential of CD105 + MSCs was demonstrated. 5-AZ induced increased expression of sarcomeric proteins without complete sarcomere organization. Treated cells also showed increased presence of connexin-43 both in young and old donor-derived cells. Intercellular communications were verified by the observation of gap junctions and passage of Ca 2+ between neighbouring cells. Spontaneous Ca 2+ raises did not significantly increase after 5-AZ treatment in both age groups. Conclusion: Age does not influence the adipogenic and myogenic differentiation potential of human CD105 + MSCs.

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