Angiopoietin-like protein 2 inhibits thrombus formation.

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Tác giả: Changlong Bi, Alex C Y Chang, Yuqi Fan, Lingyu Guo, Qing He, Dongsheng Liu, Jin Wang, Junfeng Zhang, Kandi Zhang, Mingliang Zhang, Peng Zhang, Tiantian Zhang

Ngôn ngữ: eng

Ký hiệu phân loại: 668.43 Protein plastics

Thông tin xuất bản: Netherlands : Molecular and cellular biochemistry , 2025

Mô tả vật lý:

Bộ sưu tập: NCBI

ID: 173895

Acute myocardial infarction is mainly caused by a lack of blood flood in the coronary artery. Angiopoietin-like protein 2 (ANGPTL2) induces platelet activation and thrombus formation in vitro through binding with immunoglobulin-like receptor B, an immunoglobulin superfamily receptor. However, the mechanism by which it regulates platelet function in vivo remains unclear. In this study, we investigated the role of ANGPTL2 during thrombosis in relationship with ST-segment elevation myocardial infarction (STEMI) with spontaneous recanalization (SR). In a cohort of 276 male and female patients, we measured plasma ANGPTL2 protein levels. Using male Angptl2-knockout and wild-type mice, we examined the inhibitory effect of Angptl2 on thrombosis and platelet activation both in vivo and ex vivo. We found that plasma and platelet ANGPTL2 levels were elevated in patients with STEMI with SR compared to those in non-SR (NSR) patients, and was an independent predictor of SR. Angptl2 deficiency accelerated mesenteric artery thrombosis induced by FeCl
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