Figure 5.
Exposure to young blood fails to reverse molecular hallmarks of aging in HSCs and the BM niche.(A–C) Age-associated replication stress features in (3/24) parabiosis cohorts with (A) γH2AX/FBL immunofluorescence staining (scale bar, 10 µm), (B) Mcm4 mRNA expression levels, and (C) single-cell division kinetics (n = cells) for the indicated HSC populations. nd, not determined. (D) Age-associated mitochondrial dysfunction in (3/24) parabiosis cohorts. MMP results are expressed as relative mean fluorescence intensity (MFI) of tetramethylrhodamine-ethyl-ester (TMRE) staining for the indicated HSC populations. Experiments performed on different days were normalized to 1 for each internal Y HSC control, and then averaged together. (E) Age-associated BM niche cell deterioration in (3/24) parabiosis cohorts with frequency and colony forming activity of endosteal OPrs in the indicated mice. Data are means ± SD; *, P ≤ 0.05.

Exposure to young blood fails to reverse molecular hallmarks of aging in HSCs and the BM niche. (A–C) Age-associated replication stress features in (3/24) parabiosis cohorts with (A) γH2AX/FBL immunofluorescence staining (scale bar, 10 µm), (B) Mcm4 mRNA expression levels, and (C) single-cell division kinetics (n = cells) for the indicated HSC populations. nd, not determined. (D) Age-associated mitochondrial dysfunction in (3/24) parabiosis cohorts. MMP results are expressed as relative mean fluorescence intensity (MFI) of tetramethylrhodamine-ethyl-ester (TMRE) staining for the indicated HSC populations. Experiments performed on different days were normalized to 1 for each internal Y HSC control, and then averaged together. (E) Age-associated BM niche cell deterioration in (3/24) parabiosis cohorts with frequency and colony forming activity of endosteal OPrs in the indicated mice. Data are means ± SD; *, P ≤ 0.05.

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