Integrating microRNA and messenger RNA expression profiles in a rat model of deep vein thrombosis

Jin, Qianqian; Sun, Jun-hong; Du, Qiu-xiang; Lu, Xiaojun; Zhu, Xiyan; Fan, Haoliang; Hölscher, Christian; Wang, Ying-Yuan

doi:10.3892/ijmm.2017.3105

Cited by 28 publications

(20 citation statements)

References 43 publications

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“…Clinical manifestations of DVT are primarily lower limb swelling, ulceration, and necrosis, which may seriously limit patients' quality of life . Existing literature has highlighted the participation of miRNAs in almost all pathological and physiological processes including DVT . In this study, we established in vivo LEDVT mouse models and identified that miR‐103a‐3p might be an endogenous regulator of LEDVT.…”

Section: Discussionmentioning

confidence: 95%

“…21 Existing literature has highlighted the participation of miRNAs in almost all pathological and physiological processes including DVT. 22 In this study, we established in vivo LEDVT mouse models and identified that miR-103a-3p might be an endogenous regulator of LEDVT. Restoration of miR-103a-3p could potentially prevent LEDVT development via inhibiting CXCL12 expression.…”

Section: Mir-103a-3p Regulates Macrophage Polarization and Venous Tmentioning

confidence: 99%

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Overexpressed microRNA‐103a‐3p inhibits acute lower‐extremity deep venous thrombosis via inhibition of CXCL12

et al. 2019

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Studies have shown that microRNAs (miRNAs) participate in almost all pathological and physiological processes including acute lower‐extremity deep venous thrombosis (LEDVT). Here, this study was designed to elucidate the possible function of miR‐103a‐3p in acute LEDVT. Expression of miR‐103a‐3p and chemokine C‐X‐C motif ligand 12 (CXCL12) was initially quantified in plasma collected from 81 LEDVT patients. Then LEDVT mouse models were established by injection with 3% sodium pentobarbital. The interaction between miR‐103a‐3p and CXCL12 was identified by dual‐luciferase reporter gene assay. After gain‐ and loss‐of‐function studies, interleukin‐6 (IL‐6) and IL‐8 and tissue factor (TF) levels, and expression of plasminogen activator inhibitors (PAIs), von Willebrand factor (vWF), thromboxane A2 (TH‐A2), F4/80, IL‐12, Arginase‐1 (Arg‐1) and CD206 were determined using enzyme‐linked immunosorbent assay (ELISA), reverse transcription quantitative polymerase chain reaction (RT‐qPCR) and western blot analysis, respectively. miR‐103a‐3p was downregulated, while CXCL12 was upregulated in patients and mice with LEDVT. miR‐103a‐3p targets CXCL12 and inhibited its expression. Overexpressed miR‐103a‐3p or downregulated CXCL12 decreased expression of IL‐6, IL‐8, TF, PAIs, vWF, TH‐A2, M1 markers (IL‐6 and IL‐12), yet increased expression of M2 markers (Arg‐1 and CD206) in LEDVT mice. Additionally, upregulated miR‐103a‐3p or silencing CXCL12 suppressed thrombosis in LEDVT mice. However, overexpression of CXCL12 reversed the tendency mentioned above. Altogether, miR‐103a‐3p can potentially downregulate CXCL12 expression to disrupt inflammatory response and thrombosis, ultimately preventing the development of LEDVT. Our findings underscore a possible alternative therapeutic strategy to limit LEDVT.

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Section: Discussionmentioning

confidence: 95%

Section: Mir-103a-3p Regulates Macrophage Polarization and Venous Tmentioning

confidence: 99%

Overexpressed microRNA‐103a‐3p inhibits acute lower‐extremity deep venous thrombosis via inhibition of CXCL12

et al. 2019

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“…The rats were randomly divided into three groups (n = 10 per group): a control group, a DVT group, and a sham group. According to our previous study 33 , the rats in the DVT group were anesthetized with 10% chloral hydrate. After exploring the IVC, all side branches were ligated.…”

Section: Methodsmentioning

confidence: 99%

Comparison of the serum metabolic signatures based on 1H NMR between patients and a rat model of deep vein thrombosis

Cao

Jin

Wang

et al. 2018

Sci Rep

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Deep vein thrombosis (DVT) and pulmonary embolism (PE) have high morbidity, reduce quality of life, and can cause death. Biomarkers or genetic risk factors have not been identified in patients with DVT. In present study, serum of 61 patients suffering from DVT and a rat DVT model (n = 10) were assayed by a proton nuclear magnetic resonance (1H NMR) metabolomics technique combing with multivariate statistical analysis to identify the metabolites. The MetPA platform was used to identify differences in the metabolic pathways between the rat model and patients. The metabolomics results discovered that 11 different metabolites in rats and 20 different metabolites in DVT patients. Seven metabolites both altered in the rats and patients. Moreover, we observed changes in the metabolic pathways, including carbohydrate metabolism, lipid metabolism, and amino acid metabolism that were induced immediately by the thrombosis. Pathway of aminoacyl-tRNA biosynthesis perturbed only in the patients which was associated with the genetic risk factor of DVT. The study demonstrated that serum 1H NMR metabolomics can be used to diagnose DVT in the clinic. The altered pathways related to thrombosis and genetics will provide a foundation and new strategies for understanding the pathological mechanism and pharmacological targets of DVT.

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“…The level of the miRNA-17-92 cluster increases 24 h after coronary occlusion [14]. In addition, miR-92a-3p is upregulated in the vascular tissues in a rat model of deep vein thrombosis [15]. miR-92a-3p is very sensitive to changes in shear stress.…”

Section: Introductionmentioning

confidence: 99%

Role of miR-92a-3p, oxidative stress, and p38MAPK/NF-κB pathway in rats with central venous catheter related thrombosis

Gan

Zhao

Yan

et al. 2020

BMC Cardiovasc Disord

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Background: miR-92a-3p and oxidative stress are reportedly associated with venous thrombosis. However, the role of miR-92a-3p and oxidative stress in catheter-related thrombosis (CRT) remains ambiguous. Herein, we studied the roles of miR-92a-3p, oxidative stress, and p38-mitogen-activated protein kinase/nuclear factor kappa-B (MAPK/NF-κB) pathway in CRT. Methods: Forty-five male rats were randomly and equally divided into control, sham operation, and CRT groups. The rats were sacrificed after 10 days. Reactive oxygen species (ROS), superoxide dismutase (SOD), and malondialdehyde (MDA) levels in the serum were determined by enzyme-linked immunosorbent assay (ELISA). The expression levels of miR-92a-3p, heme oxygenase-1 (HO-1), NF-κB p65, and p38 MAPK in the venous tissues were detected with quantitative polymerase chain reaction (qPCR) and Western blot. Results: Thrombosis was observed only in the CRT group. Compared with the levels in the control and sham operation groups, ROS and MDA significantly increased in the CRT group, but SOD significantly decreased. qPCR and Western blot results showed that miR-92a-3p, HO-1, p38 MAPK, and NF-κB p65 expression was significantly upregulated in the venous tissues of the CRT group. Moreover, miR-92a-3p was positively correlated with HO-1, which was positively correlated with p38 MAPK and NF-κB p65. Conclusion: miR-92a-3p was correlated with oxidative stress in CRT. miR-92a-3p and oxidative stress contributed to endothelial dysfunction and simultaneously was associated with CRT.

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Integrating microRNA and messenger RNA expression profiles in a rat model of deep vein thrombosis

Cited by 28 publications

References 43 publications

Overexpressed microRNA‐103a‐3p inhibits acute lower‐extremity deep venous thrombosis via inhibition of CXCL12

Overexpressed microRNA‐103a‐3p inhibits acute lower‐extremity deep venous thrombosis via inhibition of CXCL12

Comparison of the serum metabolic signatures based on 1H NMR between patients and a rat model of deep vein thrombosis

Role of miR-92a-3p, oxidative stress, and p38MAPK/NF-κB pathway in rats with central venous catheter related thrombosis

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