Protease-Activated Receptor 1 Contributes to Angiotensin II-Induced Cardiovascular Remodeling and Inflammation

Antoniak, Silvio; Cardenas, Jessica C.; Buczek, Laura; Church, Frank C.; Mackman, Nigel; Pawliński, Rafał

doi:10.1159/000452269

Cited by 32 publications

(25 citation statements)

References 68 publications

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“…Notably, this receptor cannot be activated by C3a [ 39 ]. Activation of PAR1 and 4 by C4a leads to cellular activation and enhanced endothelial permeability [ 39 ], and PAR1 has been previously implicated in, e.g., cardiac remodeling [ 40 ] and hepatic injury [ 43 ]. Notably, C4a cannot signal via the C3aR [ 41 ].…”

Section: Discussionmentioning

confidence: 99%

Complement C3 and C4, but not their regulators or activated products, are associated with incident metabolic syndrome: the CODAM study

et al. 2018

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PurposeWe investigated the associations of components of the alternative (C3, C3a, Bb, factor D [FD], factor H [FH], properdin) and the classical complement pathway (C4, C1q, C1-inhibitor [C1-INH]) with prevalent and incident metabolic syndrome in a cohort with a moderately increased risk of cardiometabolic disease.MethodsThe study cohort was comprised of 574 participants (61% men, age 59.6 ± 7.0 years) at baseline and 489 participants after 7-year follow-up. Multiple logistic regression analyses were done to investigate the associations of concentrations of baseline plasma complement (standardized values) with prevalent and incident (in those without metabolic syndrome at baseline, n = 189) metabolic syndrome.ResultsC3 (odds ratio (OR) = 1.48 [95% confidence interval: 1.02; 2.14]) and C4 (OR = 1.95 [1.32; 2.88]), but none of the other complement components were associated with incident metabolic syndrome (n = 40 cases). Notably, in the cross-sectional analyses, we did observe higher levels of C3a (OR = 1.25 [1.03; 1.52]), FH (OR = 2.93 [2.24; 3.83]), and properdin (OR = 1.88 [1.50; 2.34]), in addition to C3 (OR = 3.60 [2.73; 4.75]) and C4 (OR = 1.39 [1.13; 1.69]), in those with the metabolic syndrome compared to those without, while no association was observed for FD, Bb, C1q, or C1-INH.ConclusionsIn the cross-sectional analyses, the effects sizes (standardized regression coefficients) for C3 and C4 were similar to those of (some of) the regulators and activators, yet only C3 and C4 were associated with incident disease. These findings suggest a role for C3 and C4, but not their regulators or activated products, in the development of the metabolic syndrome.

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Section: Discussionmentioning

confidence: 99%

Complement C3 and C4, but not their regulators or activated products, are associated with incident metabolic syndrome: the CODAM study

et al. 2018

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“…5B and C). Previous studies have reported crosstalk between coagulation and inflammation (Antoniak et al2016(Antoniak et al , 2013(Antoniak et al , 2016aAndrade et al 2013;Wilson et al 2014;Azeredo et al 2015;Yang and Tang 2016). Therefore, we determined if anticoagulation affected the recruitment of…”

Section: Anticoagulation Does Not Affect Viral Genomes or Inflammationmentioning

confidence: 93%

“…Total lung RNA was extracted using TRIzol (Life Technologies, Carlsbad, CA). RNA was reverse transcribed into cDNA using the iScript ™ RT Supermix (Bio-Rad) and the levels of H1N1 PR/8 genomes were quantified by realtime PCR using SSoFast ™ Probes Supermix and a Bio-Rad cycler (Bio-Rad) as described (Antoniak et al 2016(Antoniak et al , 2013(Antoniak et al , 2016a. Rpl4 was used for normalization.…”

Section: Rna Isolation and Rt-pcrmentioning

confidence: 99%

Anticoagulation increases alveolar hemorrhage in mice infected with influenza A

Tatsumi

Antoniak

Gondouin

et al. 2016

Physiological Reports

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Influenza A virus infection is a common respiratory tract infection. Alveolar hemorrhage has been reported in patients with influenza pneumonia and in mice infected with influenza A. In this study, we investigated the effect of two anticoagulants on alveolar hemorrhage after influenza A virus (IAV) infection of wild‐type mice. Wild‐type mice were anticoagulated with either warfarin or the direct thrombin inhibitor dabigatran etexilate and then infected with a mouse‐adapted influenza virus (A/Puerto Rico/8/34 H1N1). Alveolar hemorrhage was assessed by measuring hemoglobin levels in the bronchoalveolar lavage fluid (BALF). We also measured vascular permeability and viral genomes in the lung, as well as white blood cells, inflammatory mediators, and protein in BALF. Survival and body weight were monitored for 14 days after influenza A infection. In infected mice receiving either warfarin or dabigatran etexilate we observed decreased activation of coagulation in the BALF and increased alveolar hemorrhage. Warfarin but not dabigatran etexilate increased vascular permeability and mortality of influenza A‐infected mice. Anticoagulation did not affect levels of influenza A genomes, white blood cells, inflammatory mediators, or protein in the BALF. Our study indicates that systemic anticoagulation increases alveolar hemorrhage in influenza A‐infected mice.

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“…First, it up-regulates tissue factor and levels of plasminogen activator inhibitor 1. Second, it reduces antithrombotic proteins as antithrombin III [ 103 , 104 ].…”

Section: Dendritic Cell and Hypercoagulabilitymentioning

confidence: 99%

Dendritic Cells and SARS-CoV-2 Infection: Still an Unclarified Connection

Caldarola

Parisi

Leosco

et al. 2020

Cells

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The ongoing pandemic due to Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) has so far infected about 2.42 × 107 (as at 27 August 2020) subjects with more than 820,000 deaths. It is the third zoonotic coronavirus-dependent outbreak in the last twenty years and represents a major infective threat for public health worldwide. A main aspect of the infection, in analogy to other viral infections, is the so-called “cytokine storm”, an inappropriate molecular response to virus spread which plays major roles in tissue and organ damage. Immunological therapies, including vaccines and humanized monoclonal antibodies, have been proposed as major strategies for prevention and treatment of the disease. Accordingly, a detailed mechanistic knowledge of the molecular events with which the virus infects cells and induces an immunological response appears necessary. In this review, we will report details of the initial process of SARS-CoV-2 cellular entry with major emphasis on the maturation of the spike protein. Then, a particular focus will be devoted to describe the possible mechanisms by which dendritic cells, a major cellular component of innate and adaptive immune responses, may play a role in the spread of the virus in the human body and in the clinical evolution of the disease.

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Protease-Activated Receptor 1 Contributes to Angiotensin II-Induced Cardiovascular Remodeling and Inflammation

Cited by 32 publications

References 68 publications

Complement C3 and C4, but not their regulators or activated products, are associated with incident metabolic syndrome: the CODAM study

Complement C3 and C4, but not their regulators or activated products, are associated with incident metabolic syndrome: the CODAM study

Anticoagulation increases alveolar hemorrhage in mice infected with influenza A

Dendritic Cells and SARS-CoV-2 Infection: Still an Unclarified Connection

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