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Updated: Jul 13, 2026
Mouse Complete Stasis Model of Inferior Vena Cava Thrombosis
Published on: June 15, 2011
Inhibiting MMP13 Attenuates Deep Vein Thrombosis in a Mouse Model by Reducing the Expression of Pdpn
Ji Luo1, Jin Zhou2, Jing-Zeng Luo3
1Department of Intensive Care Unit, The First People's Hospital of Ziyang, Ziyang, 641300, China.
Objective:
Matrix metalloproteinase 13 (MMP13) is an extracellular matrix protease that affects the progression of atherosclerotic plaques and arterial thrombi by degrading collagens, modifying protein structures and regulating inflammatory responses, but its role in deep vein thrombosis (DVT) has not been determined. The purpose of this study was to investigate the potential effects of MMP13 and MMP13-related genes on the formation of DVT.
Methods:
We altered the expression level of MMP13 in vivo and conducted a transcriptome study to examine the expression and relationship between MMP13 and MMP13-related genes in a mouse model of DVT. After screening genes possibly related to MMP13 in DVT mice, the expression levels of candidate genes in human umbilical vein endothelial cells (HUVECs) and the venous wall were evaluated. The effect of MMP13 on platelet aggregation in HUVECs was investigated in vitro.
Results:
Among the differentially expressed genes, interleukin 1 beta, podoplanin (Pdpn), and factor VIII von Willebrand factor (F8VWF) were selected for analysis in mice. When MMP13 was inhibited, the expression level of PDPN decreased significantly in vitro. In HUVECs, overexpression of MMP13 led to an increase in the expression level of PDPN and induced platelet aggregation, while transfection of PDPN-siRNA weakened the ability of MMP13 to increase platelet aggregation.
Conclusions:
Inhibiting the expression of MMP13 could reduce the burden of DVT in mice. The mechanism involves downregulating the expression of Pdpn through MMP13, which could provide a novel gene target for DVT diagnosis and treatment.
Insights
Matrix metalloproteinase 13 (MMP13) inhibition reduces deep vein thrombosis (DVT) burden in mice. This occurs by downregulating podoplanin (PDPN) expression, offering a potential new therapeutic target for DVT.
Area of Science:
- Biochemistry
- Molecular Biology
- Vascular Biology
Background:
- Matrix metalloproteinase 13 (MMP13) degrades extracellular matrix components, influencing atherosclerosis and thrombosis.
- The specific role of MMP13 in deep vein thrombosis (DVT) formation remains largely uncharacterized.
Purpose of the Study:
- To investigate the role of MMP13 and related genes in DVT development.
- To explore MMP13 as a potential therapeutic target for DVT.
Main Methods:
- MMP13 expression was manipulated in a mouse DVT model.
- Transcriptome analysis identified MMP13-related genes.
- Gene expression was validated in human umbilical vein endothelial cells (HUVECs) and venous walls.
- In vitro assays assessed MMP13's effect on platelet aggregation.
Main Results:
- Interleukin 1 beta, podoplanin (PDPN), and factor VIII von Willebrand factor (F8VWF) were identified as key genes.
- MMP13 inhibition significantly decreased PDPN expression in vitro.
- MMP13 overexpression in HUVECs increased PDPN levels and induced platelet aggregation.
- PDPN knockdown attenuated MMP13-induced platelet aggregation.
Conclusions:
- Inhibiting MMP13 expression reduces DVT burden in a murine model.
- The mechanism involves MMP13-mediated downregulation of PDPN.
- MMP13 and PDPN represent potential novel targets for DVT diagnosis and treatment.
