Endothelial Progenitor Cells (EPC) support neovascularization and regeneration of injured endothelium both by providing a proliferative cell pool capable of differentiation into mature vascular endothelial cells and by secretion of angiogenic growth factors.
An alternative way to remove damaged cells from the active stem cell pool is the engagement of differentiation.
Nelson and Nusse (2004) [4] provided a conceptual framework for intersection of these β-catenin pools in the context of differentiation and development.
Moreover, the role of NG2 cell as oligodendrocyte progenitors, differentiating when re-myelination is needed [ 30, 61], inevitably leads to the speculation that alterations in this population pool or even a failure of differentiation due to microglial activation [ 38, 39] could potentially in part underlie the oligodendrocyte loss and white matter damage found in AD patients.
These results imply that reducing unphosphorylated Id2 may improve the pool of myoblasts available for differentiation by increasing proliferation and inhibiting apoptosis.
In response to muscle injury, satellite cells are activated, proliferate to form a pool of myoblasts, commit to differentiation and then fuse together to repair or replace damaged muscle fibres (reviewed, [8]).
Colon cancer is known to be a relatively heterogeneous tumour, and is characterised by a heterogenic pool of cells with distinct differentiation patterns.
However, the seed bank had greater levels of differentiation among pools (beta diversity; β) than aboveground samples.
Given that the co-localization of the two proteins increased substantially in fibers treated with the proteasome inhibitor, as determined by the co-localization coefficient (Fig. 4B and D), we can infer that Ozz regulates the proteasomal degradation of a selected pool of sarcomeric MyHCemb during myofiber differentiation.
Proliferation determines the pool of muscle cells available for differentiation and thus it influences the potential for muscle growth.
