Characteristics of the complement system gene expression deficiency in patients with symptomatic pulmonary embolism

Lv, Wei; Wang, Lemin; Duan, Qianglin; Gong, Zhu; Yang, Fan; Song, Haoming; Song, Yanli

doi:10.1016/j.thromres.2013.04.027

Cited by 6 publications

(5 citation statements)

References 19 publications

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“…[77][78][79][80][81][82][83][84][85] Among the 10 studies on ischaemic stroke, 8 investigated associations between lectin pathway proteins and occurrence of stroke (case-control design), [86][87][88][89][90][91][92]95 and 6 of the 10 studies investigated associations between lectin pathway proteins and stroke severity and/or functional outcome in existing stroke (prospective or cross-sectional design). [88][89][90][92][93][94] The majority of studies (n ¼ 33) included MBL serum/ plasma levels and/or MBL2 genotype, while nine studies investigated one or more MASPs, 45,61,73,76,84,85,94,95,100 seven studies one or more ficolins, 41,72,73,83,86,88,92 five studies MAp44 45,73,83,84,95 and one investigated CL-K1. 102 Studies including MBL2 genotype all investigated polymorphisms in codon 52, 54 a...…”

Section: Resultsmentioning

confidence: 99%

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The Lectin Pathway in Thrombotic Conditions—A Systematic Review

Larsen

Hvas

2018

Thromb Haemost

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The lectin pathway of the complement system can activate the coagulation system in vitro, but the role of the lectin pathway in haemostatic activation and thrombosis in vivo is not clear. We performed a systematic review of the existing literature on associations between the lectin pathway and arterial and venous thrombosis, in accordance with the Assessing the Methodological Quality of Systematic Reviews guidelines. PubMed and Embase were searched from January 1990 to March 2017. We included original studies on human study populations investigating associations between the lectin pathway (protein serum levels, genotype or gene expression) and thrombotic conditions or laboratory coagulation markers. Exclusion criteria were case studies including fewer than five cases, conference abstracts or any other language than English. In total, 43 studies were included which investigated associations between the lectin pathway and cardiovascular thrombotic events (CVEs) ( = 22), ischaemic stroke ( = 9), CVE and stroke ( = 1) and other conditions (systemic lupus erythematosus [ = 6], sepsis-related coagulopathy [ = 3], pulmonary embolism [ = 1], asparaginase treatment [ = 1]). Studies on the lectin pathway and CVE risk reported discrepant results, as both high and low mannose-binding lectin (MBL) serum levels were found to correlate with increased CVE risk. In ischaemic stroke patients, occurrence of stroke as well as increased stroke severity and poor outcome were consistently associated with high serum MBL. For other thromboembolic conditions, only few studies were identified. In conclusion, lectin pathway activation may negatively influence outcome after ischaemic stroke and possibly contribute to CVE risk. Further research is warranted to elucidate the role of the lectin pathway in other thrombotic conditions.

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Section: Resultsmentioning

confidence: 99%

“…Lv et al conducted a case-control study in patients with pulmonary embolism and healthy controls and extensively investigated complement-related messenger ribonucleic acid (mRNA) expression. 100 They found lower expression of MBL2 and MASP2 mRNA in patients with pulmonary embolism compared with healthy controls.…”

Section: Other Studiesmentioning

confidence: 94%

The Lectin Pathway in Thrombotic Conditions—A Systematic Review

Larsen

Hvas

2018

Thromb Haemost

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“…However, these studies do not provide evidence for a causative mechanism between complement activation and VTE. With respect to pulmonary embolism, mRNA expressions of complement components, receptors and regulators were shown to be unbalanced, suggesting dysfunction of the complement system (Lv et al, 2013).…”

Section: Venous Thromboembolismmentioning

confidence: 99%

Complement, inflammation and thrombosis

Rawish

Sauter

Nording

et al. 2021

British J Pharmacology

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A mutual relationship exists between immune activation and mechanisms of thrombus formation. In particular, elements of the innate immune response such as the complement system can modulate platelet activation and subsequently thrombus formation. Several components of the complement system including C3 or the membrane attack complex have been reported to be associated with platelets and become functionally active in the micromilieu of platelet activation. The exact mechanisms how this interplay is regulated and its consequences for tissue inflammation, damage or recovery remain to be defined. This review addresses the current state of knowledge on this topic and puts it into context with diseases featuring both thrombosis and complement activation. Linked Articles This article is part of a themed issue on Canonical and non‐canonical functions of the complement system in health and disease. To view the other articles in this section visit http://onlinelibrary.wiley.com/doi/10.1111/bph.v178.14/issuetoc

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“…Seven genes (CD46, CR1, CR2, C5, CFH, C1QB and SERPING1) are involved in complement activation. Three genes (CR1, C5, and C1QB) were also found to be differentially expressed in peripheral blood mononuclear cells in an independent study comparing patients with pulmonary embolism to patients with ischemic heart disease [38]. Two of the differentially expressed genes we identified in the complement cascade have been linked to thrombotic disorders.…”

Section: Discussionmentioning

confidence: 97%

Whole blood gene expression profiles distinguish clinical phenotypes of venous thromboembolism

Lewis

Suchindran

Beckman

et al. 2015

Thrombosis Research

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Introduction Recurrent venous thromboembolism (VTE) occurs infrequently following a provoked event but occurs in up to 30% of individuals following an initial unprovoked event. There is limited understanding of the biological mechanisms that predispose patients to recurrent VTE. Objectives To identify whole blood gene expression profiles that distinguished patients with clinically distinct patterns of VTE. Patients/Methods We studied 107 patients with VTE separated into 3 groups: (1) ‘low-risk’ patients had one or more provoked VTE; (2) ‘moderate-risk’ patients had a single unprovoked VTE; (3) ‘high-risk’ patients had ≥2 unprovoked VTE. Each patient group was also compared to twenty-five individuals with no personal history of VTE. Total RNA from whole blood was isolated and hybridized to Illumina HT-12 V4 Beadchips to assay whole genome expression. Results Using class prediction analysis, we distinguished high-risk patients from low-risk patients and healthy controls with good receiver operating curve characteristics (AUC = 0.81 and 0.84, respectively). We also distinguished moderate-risk individuals and low-risk individuals from healthy controls with AUC’s of 0.69 and 0.80, respectively. Using differential expression analysis, we identified several genes previously implicated in thrombotic disorders by genetic analyses, including SELP, KLKB1, ANXA5, and CD46. Protein levels for several of the identified genes were not significantly different between the different groups. Conclusion Gene expression profiles are capable of distinguishing patients with different clinical presentations of VTE, and genes relevant to VTE risk are frequently differentially expressed in these comparisons.

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Characteristics of the complement system gene expression deficiency in patients with symptomatic pulmonary embolism

Abstract: In PE patients, the mRNA expressions of complement components, receptors and regulators were unbalanced, suggesting dysfunction and/or deficiency of the complement system, which leads to decreased function of MAC-induced cell lysis in PE patients finally.

Cited by 6 publications

References 19 publications

The Lectin Pathway in Thrombotic Conditions—A Systematic Review

The Lectin Pathway in Thrombotic Conditions—A Systematic Review

Complement, inflammation and thrombosis

Whole blood gene expression profiles distinguish clinical phenotypes of venous thromboembolism

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