Review of the Article on Sustained Angiogenesis - Paper Example

Article full citation: Nor, J., Christensen, J., Liu, J., Peters, M., Mooney, D., Strieter, R., & Polverini, P. (2011). Upregulation of Bcl-2 in Microvascular Endothelial Cells Enhances Intratumoral Angiogenesis and Accelerates Tumor Growth. Cancer Research, 61, 2183-2188.

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In the article cited above, the authors attempt to explain the role of increased Bcl-2 expression on the acceleration of tumor growth and the sustenance of intra-tumor angiogenesis. The authors begin by describing the various factors that up-regulate the expression of Bcl-2, including the vascular endothelial growth factor (VEGF) and stimulatory chemokines such as interleukin-8 and their role in tumor growth. According to their account, by up-regulating Bcl-2, the VEGF enhances the chances of survival of the endothelial cells of infected tumor tissues. With this knowledge at hand, they establish the stimulatory effect of over-expression of Bcl-2 and the attenuation effect of IL-8 neutralization of antibodies on the increased angiogenic potential of these cells. The establishment helps this that human dermal microvascular endothelial cells (HDMECs) that have been seeded in biodegradable sponges can be implanted into human microvessels that are functional and capable of transporting mouse blood cells.

To accomplish this goal an experimental technique is involved using mice. They used the methods of construction of retroviral vector and the transduction of the human dermal microvascular endothelial cells (HDMEC). They then conducted capillary tube assays of proliferated endothelial cells and finally determined the angiogenic activity of the HDMEC using the rat corneal micro pocket assay. The HDMECs were also transfected with Bcl-2 antisense ODN. The results obtained regarding the sustenance of the angiogenic capacity of the test factors were recorded. Other methods such as the Western blot, ELISA, and the passive immunization were carried out to determine the ability of Bcl-2 to accelerate the angiogenic capacity of the tumor cells in mice. The incubation of the cells was done after approximately 48 hours at a temperature of about 37 degrees. The newly infected mice were kept for 3 weeks after which they were killed and the sponges were retrieved for further analysis.

They found out that, tumors that had high concentrations of HDMEC-Bcl-2 were more vascular compared to their counterparts only control HDMEC. The infection with anti-IL- 8 antibodies resulted in decreased microvascular density of the intra-tumor resulting into reduced tumor growth. The anti-IL-8 antibodies partially blocked the cell proliferation and sprouting of the tumor cells depending on the dose administered. It was concluded that the addition of the anti-IL-8 antibodies attenuates the expression of HDMEC-Bcl-2 and that IL-8 plays a significant role in mediating the neovascularization induced by the over-expression of Bcl-2 in the endothelial cell of tumor infected tissues.

The results and their analysis tend to justify angiogenesis as a characteristic hallmark of all cancers. In all cells infected with tumors, there is the expression of Bcl-2 and the other stimulatory factors. The over-expression of the Bcl-2 factor results in the survival of the endothelial cells. Therefore, despite the tumoral environment constraints, these cells remain viable and tend to operate normally. The availability of the tumor-derived VEGF, which are presented in all tumor cells support this growth. Also, the over-expression of Bcl-2 results in increased amounts of the stimulatory chemokine IL-8 which also induces angiogenesis. The two functions played by the Bcl-2 contribute primarily to sustained angiogenesis in the growth of tumors.