Fig. 3 Ca2+/hypoxia stimulated the proliferation of hUCB-MSCs via the HIF-1α-dependent pathway.
Plain spherical particles that were 50 and 90 nm in diameter slightly stimulated the proliferation of PC-3 cells.
Only a small selection of films (especially those containing elastin fibres) specifically stimulated the proliferation of keratinocytes, but not fibroblasts.
The r-αCS stimulated the proliferation of splenocytes from the immunized mice upon re-induction by the antigen, in vitro.
In a cell proliferation assay, both A-PRF and CGF extracts significantly stimulated the proliferation of human periosteal cells without significant reduction at higher doses.
Osteogenic cells that were co-cultured with chondrogenic cells (in the chondral layer) showed higher cellularity over time, suggesting that chondrogenic cells stimulated the proliferation of osteogenic cells.
Fibroblast growth factor-2 (FGF-2) stimulated the proliferation of these immature cells and the subsequent production of mineralized calcium was induced by β-glycerophosphate treatment.
The addition of SP stimulated the proliferation of synovial fibroblastic cells and this effect was inhibited by SP or NK1-R antagonists.
To test biological responses of human bone marrow derived MSC due to copper ions, we found that copper stimulated the proliferation of MSC in a narrow concentration range around 0.1 mM.
IGF-I gene expression stimulated the proliferation of C2C12 cells, and a significant increase in the growth rate was observed for IGF-I-transduced C2C12 cells with Dox addition, designated C2C12/IGF (Dox+) cells.
With the specific Si ion and its effective concentrations, CS extracts stimulated the proliferation of HUVECs, up-regulated the expression of vascular endothelial growth factor, basic fibroblast growth factor and their receptors, and finally stimulated the proangiogenesis.
