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16.11.2017 | Original Article | Ausgabe 1/2018

Immunologic Research 1/2018

Long-term presence of angiotensin II type 1 receptor autoantibody reduces aldosterone production by triggering Ca2+ overload in H295R cells

Immunologic Research > Ausgabe 1/2018
Jinghui Lei, Suli Zhang, Pengli Wang, Yang Liao, Jingwei Bian, Xiaochen Yin, Ye Wu, Lina Bai, Feng Wang, Xiaoli Yang, Huirong Liu
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Electronic supplementary material

The online version of this article (https://​doi.​org/​10.​1007/​s12026-017-8963-6) contains supplementary material, which is available to authorized users.


Preeclamptic women are reported to have inadequate plasma volume expansion coupled with a suppressed secretion of aldosterone; however, the specific mechanism of preeclampsia remains unclear. We demonstrated that the presence of long-term angiotensin II type 1 receptor autoantibody (AT1-AA) reduces aldosterone production by triggering a Ca2+ overload in H295R cells. AT1-AA was discovered in preeclamptic women and reported to activate AT1R, and consequently elevate intracellular Ca2+. We found that AT1-AA significantly prolonged the time of intracellular Ca2+ elevation. Besides promoting aldosterone production as a second messenger, Ca2+ overload shows a cytotoxic effect. Our data reveals that long-term presence of AT1-AA triggered a Ca2+ overload and consequent impairment of aldosterone production, which could be prevented by a PKC inhibitor, Gö 6983, or a calcium channel inhibitor, nifedipine. These findings have clinical significance because AT1R blockers are not recommended for treatment of preeclampsia due to their potential harm to the fetus. Our findings also emphasize a potential clinical benefit of immunoadsorption or neutralization of AT1-AA in preeclamptic women.

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