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Isolating Mesangiogenic Progenitor Cells MPCs from Human Bone Marrow
Published on: July 15, 2016
Age-Related Changes in FGF-2, Fibroblast Growth Factor Receptors and β-Catenin Expression in Human Mesenchyme-Derived
Marja M Hurley1, Gloria Gronowicz2, Li Zhu3
1Department of Medicine, UCONN Health, Farmington, CT.
Abstract:
FGF-2 stimulates preosteoblast replication, and knockout of the FGF-2 gene in mice resulted in osteopenia with age, associated with decreased Wnt-β-Catenin signaling. In addition, targeted expression of FGF-2 in osteoblast progenitors increased bone mass in mice via Wnt-β-Catenin signaling. We posited that diminution of the intrinsic proliferative capacity of human mesenchyme-derived progenitor cells (HMDPCs) with age is due in part to reduction in FGF-2. To test this hypothesis HMDPCs from young (27-38), middle aged (47-56), and old (65-76) female human subjects were isolated from bone discarded after orthopedic procedures. HMDPCs cultures were mostly homogeneous with greater than 90% mesenchymal progenitor cells, determined by fluorescence-activated cell sorting. There was a progressive decrease in FGF-2 and FGFR1 mRNA and protein in HMDPCs with age. Since FGF-2 activates β-catenin, which can enhance bone formation, we also assessed its age-related expression in HMDPCs. An age-related decrease in total-β-Catenin mRNA and protein expression was observed. However there were increased levels of p-β-Catenin and decreased levels of activated-β-Catenin in old HMDSCs. FGF-2 treatment increased FGFR1 and β-Catenin protein, reduced the level of p-β-Catenin and increased activated-β-Catenin in aged HMDPCs. In conclusion, reduction in FGF-2 expression could contribute to age-related impaired function of HMDPCs via modulation of Wnt-β-catenin signaling.
Insights
Reduced fibroblast growth factor-2 (FGF-2) contributes to age-related decline in human mesenchymal progenitor cell function. This impairment involves altered Wnt-beta-Catenin signaling, impacting bone health.
Area of Science:
- Cell Biology
- Gerontology
- Bone Biology
Background:
- Fibroblast Growth Factor-2 (FGF-2) is crucial for osteoblast replication and bone mass.
- Age-related bone loss (osteopenia) is linked to decreased Wnt-beta-Catenin signaling.
- FGF-2 expression and function may decline with age, affecting progenitor cell proliferation.
Purpose of the Study:
- To investigate the role of FGF-2 reduction in age-related functional decline of human mesenchymal-derived progenitor cells (HMDPCs).
- To determine the impact of aging on FGF-2, FGFR1, and Wnt-beta-Catenin signaling in HMDPCs.
- To assess the potential of FGF-2 to restore aged HMDPC function.
Main Methods:
- Isolation and culture of HMDPCs from young, middle-aged, and old female donors.
- Quantification of FGF-2, FGFR1, and beta-Catenin (total, phosphorylated, activated) mRNA and protein levels via RT-PCR and Western blotting.
- Assessment of HMDPC homogeneity using fluorescence-activated cell sorting (FACS).
- Treatment of aged HMDPCs with FGF-2 to evaluate functional recovery.
Main Results:
- A progressive decrease in FGF-2 and FGFR1 mRNA and protein was observed in HMDPCs with increasing age.
- Total beta-Catenin expression declined with age, accompanied by increased phosphorylated beta-Catenin and decreased activated beta-Catenin in older HMDPCs.
- FGF-2 treatment of aged HMDPCs restored FGFR1 and beta-Catenin protein levels, reduced phosphorylation, and increased beta-Catenin activation.
Conclusions:
- Reduced FGF-2 expression is a significant factor in the age-related functional impairment of HMDPCs.
- The age-related decline in HMDPC function is mediated, in part, by the modulation of Wnt-beta-Catenin signaling.
- FGF-2 supplementation holds potential for ameliorating age-associated deficits in mesenchymal progenitor cells and bone health.
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