Platelet hyaluronidase 2 enrichment in acute coronary syndromes: a conceivable role in monocyte-platelet aggregate formation.
Ramona VinciDaniela PedicinoAlessia D'AielloPellegrino CiampiMyriana PonzoAlice BonanniGiulio RussoRocco Antonio MontoneMassimo MassettiFilippo CreaGiovanna LiuzzoPublished in: Journal of enzyme inhibition and medicinal chemistry (2021)
Acute Coronary Syndromes (ACS) with plaque erosion display dysregulated hyaluronan metabolism, with increased hyaluronidase-2 (HYAL2) expression. However, the expression and the role of this enzyme on platelets has never been explored. We evaluated the platelet's HYAL2 (pltHYAL2) levels on I) stable angina (SA) and II) ACS patients, furtherly sub-grouped in Intact-Fibrous-Cap (IFC) and Ruptured-Fibrous-Cap (RFC), according to Optical Coherence Tomography. We assessed the HYAL2 role through an in vitro model setting of co-cultured monocytes and platelets, before and after treatment with low-molecular-weight hyaluronic acid (HA) as pro-inflammatory stimulus and with or without HYAL2-antibody to inhibit HYAL2 activity. ACS patients exhibit higher pltHYAL2 levels comparing to SA, with the higher expression for IFC group. The addition of HYAL2-antibody significantly reduced the percentage of monocyte-platelet binding, suggesting that pltHYAL2 enrichment at the site of the culprit lesion is a key mediator in the systemic thrombo-inflammatory status of ACS presenting with plaque erosion.
Keyphrases
- acute coronary syndrome
- hyaluronic acid
- end stage renal disease
- poor prognosis
- percutaneous coronary intervention
- dendritic cells
- newly diagnosed
- ejection fraction
- chronic kidney disease
- coronary artery disease
- prognostic factors
- optical coherence tomography
- endothelial cells
- peripheral blood
- binding protein
- peritoneal dialysis
- immune response
- coronary artery
- patient reported outcomes
- brain injury
- transcription factor
- patient reported
- drug induced