A similar experimental design was used to analyse if cells can be stimulated to migrate from native human articular cartilage by PBMCs.
These studies demonstrate that articular chondrocytes can be stimulated to migrate out of parent cartilage following single impact load and culture.
One interesting study has revealed that KRAS-mutated colorectal cancer cell lines are not only more resistant to TRAIL-induced apoptosis induction than KRAS wild-type cells, but instead are stimulated to migrate when treated with TRAIL.
We used HEK293 cells, which only poorly migrate without treatment but can be stimulated to migrate by the addition of 12-O-tetradecanoylphorbol 13-acetate (TPA), a drug that down-regulates agonist-driven Ca2+ release from the ER [ 25] and stimulates cell migration [ 26, 27].
However, increased permeability develops much more slowly in cultured endothelium and often peaks over a period of hours, suggesting that the permeability observed may reflect, at least in part, a loosening of intercellular connections as endothelial cell are stimulated to migrate by VEGF-A.
When ECs are plated onto a layer of gel matrix, they are stimulated to migrate and differentiate into tubular-like structures simulating the in vivo process [ 44].
Then, keratinocytes and fibroblasts are stimulated to proliferate and migrate over the provisional matrix, so the granulation tissue formation begins.
Following physiological stimuli, such as physical activity or muscle injury, SCs are stimulated to proliferate and to migrate to the site of injury, and there to fuse with the existing myofibres or to differentiate to form new fibres.
When resting endothelial cells are activated by an angiogenic signal, they are stimulated to release degrading enzymes allowing endothelial cells to migrate, proliferate and finally differentiate to form new vessels.
