Because yesterday I realized that p53 plays a very important role in stroke. And p53 is very important mediator in cell cycle signaling; maybe some other mediators also have some effect to stroke. So today, let us go on talking about the relationship between cell cycle and stroke.
  Ischemic neuron always accompanies with cell apoptosis and DNA damage. DNA damage up-regulate the Pim1 transcript, protein expression and kinase activity. So if we block the Pim1 gene expression or the activity of Pim1 protein, could it develop a new therapy against stroke? Yi Zhang et al. have done some efforts about this.

  The researchers cultured the primary cortical neurons purchased from CD1 mice in vitro, and testthe mRNA level of Pim1 by PCR, Pim1 and CDC25 protein expression by Western Blot. They also did some other molecular biology experiments to explain the relationship between cell cycle and Pim1. For details you can read the article published on J Neurochem 2009.
  Their findings include:
1.      DNA damage up-regulate the Pim1 level.
2.      Pim1 activity changes the CDC25A expression.
3.      NF-kB is an activator for Pim1.
4.      P53 does not take part in downstream regulation of Pim1
In one word, this article can be summarized in the chart below. The chart reveals the relationship between all targets studied in their experiments. [1]

Last time, we talked the relationship between the Pim1 and stroke. Today I want focus on another member of Pim protein family Pim2.

  One paper written by J Asano et al was published on Leukemia (vorinostat) have proved Pim2 is a novel anti-apoptotic mediator in myeloma cells.
  They cultured several human non-hematopoietic, myeloid and MM cell lines for their studies. They also used bone marrow clot sections from patients. Western Blot was used to test the expression of Pim2 protein in multi-condition. Real-time PCR and cell viability assays were also carried out to confirm their findings.
  In this paper, the authors found:
These findings suggest that when MM occurs the expression of Pim2 is up-regulated by JAK/STAT path via IL-6 and NF-kB pathway. This up-regulation induces the decrease apoptotic rate of MM cells. So there are some benefits using the Pim2 inhibitor against MM. Moreover, inhibiting IGF/PI3K pathway by PI3K/Akt inhibitors such as rapamycin gains a cooperative effect to MM. These finds figure out a new therapy against MM, maybe some new therapy can be applied in clinical.

Reference:
[1] Pim-1 kinase as activator of cell cycle pathway in neuronal death induced by DNA damage. Yi Zhang et al. J Neurochem (2010) 12(2):497-510.