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The present results show that IFNγ influences NPCs in two ways by decreasing cell proliferation and by increasing cell death.
A cell death of more than 6000 cells occurred by 5 months (Fig.4b), which was followed by a slow increase in mass size but accompanied by increasing cell death.
Additionally, inhibition of VEGFR2 signaling in cerebral ischemia and traumatic brain injury can aggravate brain injury by increasing cell death, and reducing EC proliferation [ 30- 32].
It has also been found that statins may suppress the growth of cancer cells in vitro by causing the cells to pause in the G1 phase of the mitotic cycle[ 16] and by increasing cell death[ 17].
Our own data from breast cancer cell lines, indicates that COX-2 expression inhibits apoptosis, and Celecoxib (a COX-2 inhibitor) reduces xenograft growth by increasing cell death (with no effects on cell proliferation) in a nude mouse model (Barnes et al, 2004).
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The increased proliferation of osteoblasts was apparently partly counteracted by increased cell death as shown by stronger caspase 3 signaling.
As expected, accumulation of Smad7-deficient CRC cells in S phase was accompanied by increased cell death at 48 h.
These changes were accompanied by increased cell death in the ventricular zone of Foxc1 −/− mutants as measured by TUNEL labeling.
Moreover, there was a significant reduction in the number of TuJ1-positive cells in Beclin 1 +/− mice relative to wild type, accompanied by increased cell death.
This could be explained by increased cell death due to a lack of CX3CL1 binding to CX3CR1, which served as a specific survival signal for this subset.
Notably, we observed that cell aggregation in suspension promoted cell survival while loss of adhesion of shPttg2-treated cells was followed by increased cell death (20 30%) as measured by the number of cells presenting fragmented DNA (subG1 peak).
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