The dcko gene is an oncogene that promotes the development of tumors and the maintenance of the immune system. The gene is a pseudotriploid, indicating that the cell may carry three copies of the MALAT1 locus. The DECKO plasmid was shown to successfully delete this region in bulk cells, but it did not produce any detectable cutting. Therefore, the dcko gene may exclude immune cell infiltration.
TPA treatment induced similar CD45 + hematopoietic cell infiltration and F4/80+ macrophages in the control and DCKO mice. Moreover, the levels of inflammatory chemokines were elevated by 6-15 fold, irrespective of the genotype. Inflammatory cells rely on the expression of VEGFR1, which is thought to provide a migratory signal. After TPA treatment, the DCKO mouse showed a 2.4-fold increase in VEGFR1 mRNA, while the wild type showed no significant change.
The infiltration of CD45+ hematopoietic cells was comparable in DCKO and control mice. Furthermore, both types of mice had the same F4/80 positive macrophages after TPA treatment. In addition, the levels of several inflammatory chemokines increased six to fifteenfold in both genotypes, despite their differences in gene expression. The expression level of VEGFR1 (a receptor that provides a migratory signal to inflammatory cells) increased by four-fold in DCKO and control mice. However, the expression of Vegfr2 was not affected.
After TPA treatment
DCKO mice exhibited comparable levels of CD45 + hematopoietic cell infiltration to control mice. The number of F4/80 positive macrophages was similar in DCKO and control mice. In response to TPA, the expression levels of inflammatory chemokines were increased by six to fifteenfold. The genotype did not affect the expression of VEGFR1, which is thought to provide a migratory signal to inflammatory cells. Vegfr2 mRNA did not show any differences.
Interestingly, the DCKO mice also showed a similar number of CD45 + hematopoietic cells and F4/80+ macrophages after TPA treatment. In addition, both mice displayed similar levels of inflammatory chemokines in response to TPA, and mRNA levels of VEGFR2 and VEGFR1 were increased. The mRNA for both inflammatory chemokines was also significantly different between the two genotypes.
The results from the study concluded that the TPA treatment induced CD45 + hematopoietic cells were similarly infiltrated in the DCKO and control mice. Both types of mice showed similar expressions of F4/80 positive macrophages after TPA treatment. In addition, the inflammatory chemokines were correlated with mRNA levels of VEGFR1 and Vegfr2.
The study found that the DCKO mice showed similar levels of CD45 + hematopoietic cell infiltration in response to TPA treatment. In addition, both groups had similar expressions of F4/80+ macrophages. In addition, mRNA levels of inflammatory chemokines were increased in response to TPA, and genotypes did not affect expression of inflammatory chemokines.
In the same study
Both control and DCKO mice showed similar levels of CD45 + hematopoietic cell infiltration. Both groups also showed similar levels of F4/80 positive macrophages after TPA treatment. In addition, both groups were treated with TPA and their expressions of inflammatory chemokines increased by six to fifteen fold. Unlike in DCKO mice, these inflammatory chemokines were also not affected by genotype.