Plasma von Willebrand factor level is transiently elevated in a rat model of acute myocardial infarction

Li,Yan; Li,Liqun; Dong,Fengyun; Guo,Ling; Hou,Yinglong; Hu,Hesheng; Yan,Suhua; Zhou,Xiaojun; Liao,Lin; Allen,Thaddeus D.; Liu,Ju

doi:10.3892/etm.2015.2721

Plasma von Willebrand factor level is transiently elevated in a rat model of acute myocardial infarction

Authors:
- Yan Li
- Liqun Li
- Fengyun Dong
- Ling Guo
- Yinglong Hou
- Hesheng Hu
- Suhua Yan
- Xiaojun Zhou
- Lin Liao
- Thaddeus D. Allen
- Ju Liu
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Affiliations: Children's Health Care Center, Shandong Provincial Qianfoshan Hospital, Shandong University, Jinan, Shandong 250014, P.R. China, Laboratory of Microvascular Medicine, Medical Research Center, Shandong Provincial Qianfoshan Hospital, Shandong University, Jinan, Shandong 250014, P.R. China, Department of Cardiology, Shandong Provincial Qianfoshan Hospital, Shandong University, Jinan, Shandong 250014, P.R. China, Department of Endocrinology, Shandong Provincial Qianfoshan Hospital, Shandong University, Jinan, Shandong 250014, P.R. China, G.W. Hooper Research Foundation, University of California at San Francisco, San Francisco, CA 94143‑0552, USA
Published online on: September 1, 2015 https://doi.org/10.3892/etm.2015.2721
Pages: 1743-1749
Copyright: © Li et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

The von Willebrand factor (vWF) is a plasma glycoprotein that plays an essential role in hemostasis by supporting platelet adhesion and thrombus formation in response to vascular injury. Plasma levels of vWF are an independent risk factor for patients with acute myocardial infarction (AMI); however, clinical data have demonstrated a marked variation of vWF levels in patients with AMI, the reason for which has not yet been identified. In the present study, a rat model of ST‑segment elevation AMI was established, and cardiac and peripheral blood was collected for a time‑course examination of the plasma levels of vWF and tumor necrosis factor‑α (TNF‑α). The level of vWF in the blood plasma increased, peaked at 1 h and decreased to normal levels by day 7 following AMI, while the level of TNF‑α peaked at 24 h and remained elevated until day 7. The effects of TNF‑α on vWF secretion and expression were examined in cultured human umbilical vascular endothelial cells (HUVECs). TNF‑α treatment increased vWF secretion from the HUVECs but inhibited the mRNA and protein expression of vWF in the HUVECs. These results indicate that vWF secretion from endothelial cells is transiently elevated following AMI, and then decreases as the expression of vWF is inhibited by TNF‑α. The present study increases the understanding of the pathophysiology of vWF and indicates that the determination of vWF levels may be useful in the clinical evaluation of AMI.

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