Quiescence, Stemness and Adipogenic Differentiation Capacity in Human DLK1 - /CD34 + /CD24 + Adipose Stem/Progenitor Cells.

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

• Level A · Stronger Clinical Evidence
• Level B · Emerging clinical evidence with positive signals
• Level C · Early human research exploring benefits
• Level D · Scientific groundwork from lab and animal studies
• Emerging · Emerging topic under active research

Abstract (original English)

We explore the status of quiescence, stemness and adipogenic differentiation capacity in adipose stem/progenitor cells (ASCs) ex vivo, immediately after isolation from human subcutaneous white adipose tissue, by sorting the stromal vascular fraction into cell-surface DLK1 + /CD34 - , DLK1 + /CD34 dim and DLK1 - /CD34 + cells. We demonstrate that DLK1 - /CD34 + cells, the only population exhibiting proliferative and adipogenic capacity, express ex vivo the bonafide quiescence markers p21 Cip1 , p27 Kip1 and p57 Kip2 but neither proliferation markers nor the senescence marker p16 Ink4a . The pluripotency markers NANOG, SOX2 and OCT4 are barely detectable in ex vivo ASCs while the somatic stemness factors, c-MYC and KLF4 and the early adipogenic factor C/EBPβ are highly expressed. Further sorting of ASCs into DLK1 - /CD34 + /CD24 - and DLK1 - /CD34 + /CD24 + fractions shows that KLF4 and c-MYC are higher expressed in DLK1 - /CD34 + /CD24 + cells correlating with higher colony formation capacity and considerably lower adipogenic activity. Proliferation capacity is similar in both populations. Next, we show that ASCs routinely isolated by plastic-adherence are DLK1 - /CD34 + /CD24 + . Intriguingly, CD24 knock-down in these cells reduces proliferation and adipogenesis. In conclusion, DLK1 - /CD34 + ASCs in human sWAT exist in a quiescent state, express high levels of somatic stemness

Evidence level

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

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