Apolipoprotein L Domain Containing 1 Inhibits Tissue Factor to Impede Thrombus Formation in a Rat Model of Deep Vein Thrombosis via Activating PI3K/Akt Pathway

血栓 医学 血栓形成 深静脉 PI3K/AKT/mTOR通路 癌症研究 蛋白激酶B 内科学 心脏病学 细胞生物学 信号转导 生物
作者
Yulin Liao,Jing Xie,Bihui Qu
出处
期刊:Annals of Vascular Surgery [Elsevier]
卷期号:89: 312-321 被引量:1
标识
DOI:10.1016/j.avsg.2022.10.004
摘要

Background Deep venous thrombosis (DVT) is one of the major health problems worldwide. Apolipoprotein L domain containing 1 (APOLD1) was reported to be downregulated in DVT. The present study intended to investigate whether APOLD1 affects thrombus formation in a rat model of DVT. Methods The rat model of DVT was established by inferior vena cava (IVC) stenosis. At 6 hr, 12 hr, 24 hr, and 48 hr after IVC stenosis, the gross IVC with thrombus was dissected and observed. Then, the rats were preinjected with the lentiviral overexpression vector, APOLD1-LVs, 1 hr before IVC stenosis, to evaluate the influence of APOLD1 on thrombosis in rats. The serum levels of D-dimer and TAT as well as the content of TF in IVC tissues were detected by enzyme-linked immunosorbent assay (ELISA). Results IVC stenosis resulted in thrombus formation in rats, increased serum levels of D-dimer and TAT, and decreased APOLD1 expression. APOLD1 overexpression inhibited in vivo thrombosis, reduced serum levels of D-dimer, and downregulated tissue factor (TF) activity and level. APOLD1 overexpression also increased p-PI3K and p-Akt protein levels. Conclusions APOLD1 suppresses thrombus formation in a rat model of DVT via downregulating TF expression by activating the PI3K/Akt pathway. Deep venous thrombosis (DVT) is one of the major health problems worldwide. Apolipoprotein L domain containing 1 (APOLD1) was reported to be downregulated in DVT. The present study intended to investigate whether APOLD1 affects thrombus formation in a rat model of DVT. The rat model of DVT was established by inferior vena cava (IVC) stenosis. At 6 hr, 12 hr, 24 hr, and 48 hr after IVC stenosis, the gross IVC with thrombus was dissected and observed. Then, the rats were preinjected with the lentiviral overexpression vector, APOLD1-LVs, 1 hr before IVC stenosis, to evaluate the influence of APOLD1 on thrombosis in rats. The serum levels of D-dimer and TAT as well as the content of TF in IVC tissues were detected by enzyme-linked immunosorbent assay (ELISA). IVC stenosis resulted in thrombus formation in rats, increased serum levels of D-dimer and TAT, and decreased APOLD1 expression. APOLD1 overexpression inhibited in vivo thrombosis, reduced serum levels of D-dimer, and downregulated tissue factor (TF) activity and level. APOLD1 overexpression also increased p-PI3K and p-Akt protein levels. APOLD1 suppresses thrombus formation in a rat model of DVT via downregulating TF expression by activating the PI3K/Akt pathway.
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