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Autoantibody against angiotensin AT1 receptor from preeclamptic patients enhances collagen-induced human platelet aggregation.
|Title||Autoantibody against angiotensin AT1 receptor from preeclamptic patients enhances collagen-induced human platelet aggregation.|
|Publication Type||Journal Article|
|Year of Publication||2013|
|Authors||Bai K, Wang K, Li X, Wang J, Zhang J, Song L, Wang J, Zhang S, Lau WB, Ma X, Liu H|
|Journal||Acta biochimica et biophysica Sinica|
|Date Published||2013 Sep|
Hypercoagulability, platelet activation, and thrombocytopenia are the chief characteristics of preeclampsia, but their responsible underlying molecular mechanisms remain obscure. Recent studies have demonstrated that the autoantibody against angiotensin II type 1 receptor (AT1-AA) constitutes a novel risk factor for preeclampsia. However, the role of AT1-AA in platelet activation and hypercoagulability in preeclampsia has never been investigated. In the present study, we determined whether AT1-AA promotes platelet aggregation in vitro, and dissected the potential underlying mechanisms. AT1-AA was detected by enzyme-linked immunosorbent assay. After immunoglobulin G fractions purified from the preeclamptic patient positive sera were added to platelets isolated from healthy volunteers, platelet aggregation and intracellular Ca(2+) levels were detected. AT1-AA significantly enhanced in vitro collagen-induced platelet aggregation, an effect blocked by the AT1 receptor antagonist losartan. Additionally, AT1-AA increased and maintained collagen-induced cytosolic calcium concentration throughout the experiment. We demonstrated for the first time that AT1-AA significantly promotes collagen-induced platelet aggregation through angiotensin type 1 receptor activation in vitro, potentially via increased intracellular Ca(2+) concentration, supporting AT1-AA as a potential contributor to the hypercoagulable state of preeclampsia.
|Alternate Journal||Acta Biochim. Biophys. Sin. (Shanghai)|