Correction: Pluta et al. Platelet–Leucocyte Aggregates as Novel Biomarkers in Cardiovascular Diseases. Biology 2022, 11, 224

Pluta, Kinga; Porębska, Kinga; Urbanowicz, Tomasz; Olasińska-Wiśniewska, Anna; Targoński, Radosław; Krasińska, Aleksandra; Filipiak‬, Krzysztof J.; Jemielity, Marek; Krasiński, Zbigniew

doi:10.3390/biology11111554

Cited by 4 publications

(2 citation statements)

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“…Platelet-leukocyte aggregates are associated with the release of thrombotic agents, which, as hypothesized above, lead to shorter occlusion times and increase the minimum effective NAC dose. 59…”

Section: Discussionmentioning

confidence: 99%

N-Acetyl Cysteine Prevents Arterial Thrombosis in a Dose-Dependent Manner In Vitro and in Mice

Bresette,

Ashworth,

Di Paola

et al. 2024

ATVB

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BACKGROUND: Platelet-rich thrombi occlude arteries causing fatal infarcts like heart attacks and strokes. Prevention of thrombi by current antiplatelet agents can cause major bleeding. Instead, we propose using N-acetyl cysteine (NAC) to act against the protein VWF (von Willebrand factor), and not platelets, to prevent arterial thrombi from forming. METHODS: NAC was assessed for its ability to prevent arterial thrombosis by measuring platelet accumulation rate and occlusion time using a microfluidic model of arterial thrombosis with human blood. Acute clot formation, clot stability, and tail bleeding were measured in vivo with the murine modified Folts model. The effect of NAC in the murine model after 6 hours was also measured to determine any persistent effects of NAC after it has been cleared from the blood. RESULTS: We demonstrate reduction of thrombi formation following treatment with NAC in vitro and in vivo. Human whole blood treated with 3 or 5 mmol/L NAC showed delayed thrombus formation 2.0× and 3.7× longer than control, respectively ( P <0.001). Blood treated with 10 mmol/L NAC did not form an occlusive clot, and no macroscopic platelet aggregation was visible ( P <0.001). In vivo, a 400-mg/kg dose of NAC prevented occlusive clots from forming in mice without significantly affecting tail bleeding times. A lower dose of NAC significantly reduced clot stability. Mice given multiple injections showed that NAC has a lasting and cumulative effect on clot stability, even after being cleared from the blood ( P <0.001). CONCLUSIONS: Both preclinical models demonstrate that NAC prevents thrombus formation in a dose-dependent manner without significantly affecting bleeding time. This work highlights a new pathway for preventing arterial thrombosis, different from antiplatelet agents, using an amino acid derivative as an antithrombotic therapeutic.

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Section: Discussionmentioning

confidence: 99%

N-Acetyl Cysteine Prevents Arterial Thrombosis in a Dose-Dependent Manner In Vitro and in Mice

Bresette,

Ashworth,

Di Paola

et al. 2024

ATVB

View full text Add to dashboard Cite

show abstract

“…Therefore, several studies aimed to evaluate the diagnostic accuracy of other markers combined with troponin (17). Except from commonly used, highly specific markers, currently the indexes from whole blood count analysis raise attention for cardiovascular diseases diagnosis and outcomes prediction (18,19). I believe that currently, considering prolonged life span and age-related increase in co-morbidities, the routine screening test should be more comprehensive and focused on long-term survival improvement.…”

mentioning

confidence: 99%

Troponin in non-cardiac department—finding a stray piece of puzzle?

Urbanowicz¹

2023

Ann Transl Med

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Papain ameliorates monocyte-platelet aggregate formation-mediated inflammatory responses in monocytes by upregulating miRNA-146a transcription

et al. 2022

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Background MicroRNA-146a (miRNA-146a) is a nuclear factor κB (NF-κB)-inducible and inflammation-sensitive miRNA, while papain elicits anti-inflammatory effects by inhibiting monocyte-platelet aggregate (MPA)-mediated NF-κB pathway activation in monocytes. This study aimed to demonstrate the underlying effects of papain on MPA formation-initiated miRNA-146a expression and subsequent action in monocytes. Methods THP-1 cells were exposed to papain, miRNA-146a mimic and inhibitor, NF-κB inhibitor (BAY11-7082), and platelets. Flow cytometry was used to measure the MPA formation-initiated monocyte activation. Levels of miRNA-146a, cyclooxygenase 2 (COX-2) mRNA and protein, and monocyte chemoattractant protein 1 (MCP-1) were analyzed in monocytes by RT-PCR, western blot, and ELISA. Results The NF-κB inhibitor and miRNA-146a mimics upregulated miRNA-146a expression but suppressed subsequent monocyte activation and expression of COX-2 and MCP-1. Following exposure to papain, the enhanced miRNA-146a transcription induced by MPA-formation was found along with significant inhibition of monocyte activation in a dose-dependent manner. However, the inhibitory tendency was significantly reversed by miRNA-146a inhibitors. Expression of COX-2 mRNA and protein, as well as MCP-1, was inhibited in monocytes by papain, whereas miRNA-146a inhibitors promoted COX-2 and MCP-1 expression. Conclusion Our findings suggest that papain can inhibit MPA formation-mediated expression of inflammatory mediators in activated monocytes by upregulating miRNA-146a transcription.

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Correction: Pluta et al. Platelet–Leucocyte Aggregates as Novel Biomarkers in Cardiovascular Diseases. Biology 2022, 11, 224

Abstract: The authors would like to make the following correction to the published paper [...]

Cited by 4 publications

References 1 publication

N-Acetyl Cysteine Prevents Arterial Thrombosis in a Dose-Dependent Manner In Vitro and in Mice

N-Acetyl Cysteine Prevents Arterial Thrombosis in a Dose-Dependent Manner In Vitro and in Mice

Troponin in non-cardiac department—finding a stray piece of puzzle?

Papain ameliorates monocyte-platelet aggregate formation-mediated inflammatory responses in monocytes by upregulating miRNA-146a transcription

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