Key result
Incubation with Ap4A and Ap2A induced a 1.46- and 1.16-fold increase in DNA synthesis in mechanically stressed bovine aortic endothelial cells, respectively.
Why the study?
Do adenosine dinucleotides or NO donors increase DNA synthesis in mechanically stressed bovine aortic endothelial cells?
Do adenosine dinucleotides or NO donors increase DNA synthesis in mechanically stressed bovine aortic endothelial cells?
Answers are grounded in this paper and cite their sources.
Ap4A, Ap2A, and NO donors increase DNA synthesis in mechanically stressed endothelial cells, suggesting a potential mechanism to overcome endothelial dysfunction post-angioplasty.
Rapid re-endothelialization following balloon angioplasty can reduce restenosis by inhibiting smooth muscle cell migration and proliferation. However, formation of a neointima layer following angioplasty can be inhibited due to endothelial cell dysfunction and denudation. In a companion paper, it has been illustrated that mechanical loading causes a decrease in DNA synthesis in bovine aortic endothelial cells (BAECs) thus rendering them dysfunctional. The purpose of this study was to overcome BAEC dysfunction by incubation with pharmacological agents to increase DNA synthesis. Previous studies demonstrated that the adenosine dinucleotides Ap4A and Ap2A induced nitric oxide (NO) production from BAEC while Ap3A, Ap5A and Ap6A did not. This paper demonstrates that Ap4A and Ap2A induce a 1.46- and 1.16-fold increase in DNA synthesis in mechanically stressed BAECs respectively, while Ap3A, Ap5A and Ap6A do not. Additionally, NOC-18, a slow NO release NO donor, significantly increases DNA synthesis in mechanically stressed BAECs without affecting unloaded cells. These results are consistent with NO inducing DNA synthesis in mechanically stressed BAECs.
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Woodell et al. (2003) studied Endothelial cell dysfunction following mechanical injury. Ap4A, Ap2A, and NOC-18 vs. Ap3A, Ap5A, Ap6A, or unloaded cells was evaluated on DNA synthesis (1.46-fold and 1.16-fold increase). Incubation with Ap4A and Ap2A induced a 1.46- and 1.16-fold increase in DNA synthesis in mechanically stressed bovine aortic endothelial cells, respectively.
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