Lipoprotein Lp(a) and Atherothrombotic Disease

Peña-Dı́az, Aurora de la; Izaguirre-Ávila, Raúl; Anglès-Cano, Eduardo

doi:10.1016/s0188-4409(00)00084-9

Cited by 41 publications

(21 citation statements)

References 92 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…It would be interesting to know whether there is a link between the pathogenesis of IAV infections and the synthesis of lipoprotein, which is present in human plasma in a wide range of concentrations and as numerous different isoforms (8). Both lipoprotein and PLG are synthesized in the liver.…”

Section: Discussionmentioning

confidence: 99%

Annexin II Incorporated into Influenza Virus Particles Supports Virus Replication by Converting Plasminogen into Plasmin

LeBouder

Morello

Rimmelzwaan

et al. 2008

J Virol

View full text Add to dashboard Cite

For influenza viruses to become infectious, the proteolytic cleavage of hemagglutinin (HA) is essential. This usually is mediated by trypsin-like proteases in the respiratory tract. The binding of plasminogen to influenza virus A/WSN/33 leads to the cleavage of HA, a feature determining its pathogenicity and neurotropism in mice. Here, we demonstrate that plasminogen also promotes the replication of other influenza virus strains. The inhibition of the conversion of plasminogen into plasmin blocked influenza virus replication. Evidence is provided that the activation of plasminogen is mediated by the host cellular protein annexin II, which is incorporated into the virus particles. Indeed, the inhibition of plasminogen binding to annexin II by using a competitive inhibitor inhibits plasminogen activation into plasmin. Collectively, these results indicate that the annexin II-mediated activation of plasminogen supports the replication of influenza viruses, which may contribute to their pathogenicity.

show abstract

Section: Discussionmentioning

confidence: 99%

Annexin II Incorporated into Influenza Virus Particles Supports Virus Replication by Converting Plasminogen into Plasmin

LeBouder

Morello

Rimmelzwaan

et al. 2008

J Virol

View full text Add to dashboard Cite

show abstract

“…Plasma markers that could reveal activation of coagulation/ fibrinolysis pathways are increased levels of D-dimer (5), lipoprotein (lp) (a) (6); homocysteine (7), tissue-type plasminogen activator (tPA), and plasminogen activator inhibitor-1 (PAI-1; Ref. 8).…”

Section: Introductionmentioning

confidence: 99%

Genetic and Plasma Markers of Venous Thromboembolism in Patients with High Grade Glioma

Sciacca

Ciusani

Silvani

et al. 2004

Clinical Cancer Research

View full text Add to dashboard Cite

Purpose: Deep venous thrombosis/pulmonary embolism (DVT/PE) is a frequent complication in the course of cancer, particularly in brain tumors. We investigated genetic and plasma factors possibly associated with risk of DVT/PE in patients with high-grade glioma.Experimental Design: In a case-control study, we studied polymorphisms of the genes coding for factor II (G20210A), factor V (G1691A), methylenetetrahydrofolatereductase (C677T), tissue-type plasminogen activator (tPA; insertion/deletion), plasminogen activator inhibitor-1 (PAI-1; 4G/5G), and vascular endothelial growth factor (VEGF; C936T). We also measured plasma levels of Ddimer, lipoprotein (lp) (a), homocysteine, VEGF, tPA, and PAI-1, comparing healthy control patients with patients with glioma or with patients with neurological nonneoplastic disease (multiple sclerosis).Results: Genotype frequencies of polymorphisms analyzed were similar in patients with glioma and in healthy matched population. D-dimer, lp (a), homocysteine, VEGF, tPA, and PAI-1 plasma levels were significantly higher in patients with glioma than in healthy controls, whereas patients having neurological nonneoplastic disease had plasma values of these molecules not significantly different from healthy controls. VEGF, tPA, and PAI-1 were also found at high-plasma levels in patients carrying genotypes that, in healthy controls, were associated with "low-producing" phenotypes.Conclusions: Genetic risk factors alone did not explain the high incidence of DVT/PE observed in patients with glioma. Higher plasma levels of molecules influencing the coagulation pathways indicate that the tumor itself might confer an increased risk of DVT/PE; thus, D-dimer, homocysteine, lp (a), VEGF, tPA, and PAI-1 look like good candidates to be evaluated as DVT/PE prognostic factors.

show abstract

“…Effects of high plasma lipoprotein (a) levels on tissue factor pathway inhibitor and the protein C pathway Lipoprotein-a [Lp(a)] represents an independent risk factor for cardiovascular disease (CAD) [1][2][3][4] and possibly venous thromboembolism (VTE) [5,6]. Pathophysiological mechanisms could include the delivery of cholesterol to the injured blood vessels or an impairment of the endothelial function by Lp(a) [1,3,7].…”

mentioning

confidence: 99%

“…Pathophysiological mechanisms could include the delivery of cholesterol to the injured blood vessels or an impairment of the endothelial function by Lp(a) [1,3,7]. Moreover, Lp(a) could favor platelet aggregation [8], impair fibrinolysis [3], and promote inflammation [9,10].…”

mentioning

confidence: 99%

“…The median of the Lp(a) distribution was used as the cut-off value to divide patients with low and high Lp(a). As used in previous investigations, the cut-off of 300 mg L )1 was also investigated [1,3]. Sixty-two outpatients were included in the study with gender, CAD history, VTE history, family history of CAD, and CAD risk factors comparable among patients with Lp(a) above or below the median.…”

mentioning

confidence: 99%

See 1 more Smart Citation

Effects of high plasma lipoprotein (a) levels on tissue factor pathway inhibitor and the protein C pathway

Nisio

Wolde

Meijers

et al. 2005

Journal of Thrombosis and Haemostasis

View full text Add to dashboard Cite

Lipoprotein Lp(a) and Atherothrombotic Disease

Cited by 41 publications

References 92 publications

Annexin II Incorporated into Influenza Virus Particles Supports Virus Replication by Converting Plasminogen into Plasmin

Annexin II Incorporated into Influenza Virus Particles Supports Virus Replication by Converting Plasminogen into Plasmin

Genetic and Plasma Markers of Venous Thromboembolism in Patients with High Grade Glioma

Effects of high plasma lipoprotein (a) levels on tissue factor pathway inhibitor and the protein C pathway

Contact Info

Product

Resources

About