Key result
High levels of soluble endoglin alone did not induce endothelial dysfunction in mouse aorta, as endothelium-dependent vascular function was similar to control mice.
Why the study?
Does high expression of soluble endoglin induce endothelial dysfunction in mouse aorta?
Does high expression of soluble endoglin induce endothelial dysfunction in mouse aorta?
High levels of soluble endoglin alone do not induce endothelial dysfunction in mouse aorta, suggesting it may require combination with other cardiovascular risk factors to alter endothelial function.
High soluble endoglin alone does not induce endothelial dysfunction in mice; leaves open synergistic effects with other cardiovascular risk factors.
Increased levels of a soluble form of endoglin (sEng) circulating in plasma have been detected in various pathological conditions related to cardiovascular system. High concentration of sEng was also proposed to contribute to the development of endothelial dysfunction, but there is no direct evidence to support this hypothesis. Therefore, in the present work we analyzed whether high sEng levels induce endothelial dysfunction in aorta by using transgenic mice with high expression of human sEng. Transgenic mice with high expression of human sEng on CBAxC57Bl/6J background (Sol-Eng+) and age-matched transgenic littermates that do not develop high levels of human soluble endoglin (control animals in this study) on chow diet were used. As expected, male and female Sol-Eng+ transgenic mice showed higher levels of plasma concentrations of human sEng as well as increased blood arterial pressure, as compared to control animals. Functional analysis either in vivo or ex vivo in isolated aorta demonstrated that the endothelium-dependent vascular function was similar in Sol-Eng+ and control mice. In addition, Western blot analysis showed no differences between Sol-Eng+ and control mice in the protein expression levels of endoglin, endothelial NO-synthase (eNOS) and pro-inflammatory ICAM-1 and VCAM-1 from aorta. Our results demonstrate that high levels of soluble endoglin alone do not induce endothelial dysfunction in Sol-Eng+ mice. However, these data do not rule out the possibility that soluble endoglin might contribute to alteration of endothelial function in combination with other risk factors related to cardiovascular disorders.
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Němečková et al. (2015) studied Endothelial dysfunction (n=125). High soluble endoglin expression (Sol-Eng+) vs. Age-matched littermates with low soluble endoglin was evaluated on Endothelium-dependent vasodilation in isolated aorta. High levels of soluble endoglin alone did not induce endothelial dysfunction in mouse aorta, as endothelium-dependent vascular function was similar to control mice.
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