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Fig. 2 Ca2+/hypoxia-treated hUCB-MSCs maintained their proliferation capacity in long-term culture.
Thus, Ca2+/hypoxia treatment enhanced the growth of hUCB-MSCs and maintained their proliferation capacity in long-term culture through an HIF-1α/ERK-dependent pathway.
Perplexingly, despite being more impaired than ACs or PCs, ECs maintained their proliferation regardless of the severity of injury.
On secondary cultures, canine Ad-MSCs appeared as spindle-shaped cells that were grown in a monolayer and maintained their proliferation capacity without indication of senescence.
BMP-2 and BMP-4 transduced MSC aggregates maintained their proliferation rate over 21 days while Ad.GFP cells and unmodified control cultures (not shown) decreased rate of proliferation.
Strikingly, GBM cells, grafted into Tg(hsp70l:dkk1-GFP) larvae, did not differentiate and maintained their proliferation rate as shown by the expression of Nestin, β-III-tubulin and Ki67 markers.
The doubling time of hUCB-MSCs in individual treatments increased during repeated sub-cultures, but Ca2+/hypoxia conditions enabled the hUCB-MSCs to maintain their proliferation capacity in long-term culture (Fig. 2b).
These hES cell derived hepatic progenitor cells could maintain their proliferation capacity for more than 100 days of culture in vitro, while maintaining their differentiation potential into both hepatocyte-like and cholangiocyte-like cells.
Interfering with one member of this network, like IL-6 in our study, seemed to induce counteracting signals in refractory cells, in attempt to maintain their proliferation and anti-apoptotic signaling pathways at a certain level of activation.
Uncontrolled activation of Akt is common in tumor cells with PI3K activation and is thought to play an important role in maintaining their proliferation, preventing apoptosis, and supporting processes required for the metastatic phenotype [3].
Addition of mammary epithelial growth factors, such as Epidermal Growth Factor, Fibroblast Growth Factor-2, Hepatocyte Growth Factor, and Receptor Activator for Nuclear Factor κB Ligand, or extracellular matrix proteins did not maintain their proliferation potential, neither did replating the cells to increase the mitogenic response.
