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. Author manuscript; available in PMC: 2013 Aug 18.
Published in final edited form as: Cell Tissue Res. 2012 May 25;349(2):505–515. doi: 10.1007/s00441-012-1423-7

Figure 1. ASCs lack telomerase activity and exhibit telomere attrition with continued passage.

Figure 1

(a) Telomerase activity was assessed by TRAP for ASC populations isolated from different tissues (bASC denotes breast ASC). Significant activity is shown for Adenoviral hTERT-infected ASC 8. HL-60 and iPS cells served as positive controls. BJ-GFP and a lysis buffer-only samples were used as negative controls. IC denotes 36bp internal control used to standardize sample-to-sample variation. (b) Gel-based RT-PCR to detect levels of hTERT in iPS, ASC 8, ASC 9, ASC 12s, ESCs, bASC 1, bASC 2, bASC 3, BM-MSC, and BJ fibroblasts. 18S levels were tested and included as an internal control, while the negative control refers to no template added to the reaction. (c) A TRF to examine telomere lengths shows telomere erosion in ASC 8, ASC 9, ASC 12s, bASC 1, bASC 2, and bASC 3 with increased population doubling (PD), as indicated, with BJ fibroblasts at PD 21 and PD 81 as controls for telomere loss. BJ hTERT at PD 101 shows a more uniform telomere length with less heterogeneity for short telomeres. White bars indicate overall mean telomere length. Young bASCs (d) versus aged bASCs (e) express Senescence-Associated β-galactosidase (SA-β-gal) after long-term culture. Representative images for SA-β-gal staining are shown for bASC 3 at PD 9 and for bASC 3 after 40 PDs in culture. The scale bar in (d) and (e) indicates 100μc.