| Texto completo | |
| Autor(es): |
Borba-Junior, Ivanio Teixeira
;
da Silva Barbosa, Mayck
;
Moraes, Carla Roberta Peachazepi
;
Queiroz Silva, Leticia
;
Santos, Irene
;
Benites, Bruno
;
Annichino-Bizzacchi, Joyce M.
;
Costa, Fernando Ferreira
;
De Paula, Erich Vinicius
Número total de Autores: 9
|
| Tipo de documento: | Artigo Científico |
| Fonte: | RESEARCH AND PRACTICE IN THROMBOSIS AND HAEMOSTASIS; v. 9, n. 6, p. 9-pg., 2025-08-01. |
| Resumo | |
Background: Sickle cell disease (SCD) is a condition characterized by a prothrombotic state attributed to the simultaneous activation of hemostasis and innate immunity, referred to as thromboinflammation. Previous studies have demonstrated that the podoplanin (PDPN)/C-type lectin-like receptor-2 (CLEC-2) pathway is an emerging and important element of the pathogenesis of conditions in which inflammation and thrombosis coexist, but no data is available regarding its role in SCD. Objectives: To explore the PDPN/CLEC-2 pathway in SCD and correlate it with parameters of disease severity. Methods: Fifty SCD patients (35 with SS genotype; 15 with SC genotype) and 25 healthy individuals were recruited. PDPN and CLEC-2 were assessed for both soluble and surface expression on cells and cell aggregates, along with other classical parameters of hemostasis and platelet activation. An in vitro study was performed to analyze the effect of anti-PDPN antibody on the formation of monocyte-platelet aggregates. Results: Circulating levels and expression of PDPN and CLEC-2 were higher in patients with SCD, particularly in those with genotype SS. The number of CD41+CLEC+ monocytes correlated with hemoglobin, D-dimer, von Willebrand factor, and PDPN+ monocytes. In vitro, PDPN blockade reduced both monocyte-platelet aggregate formation and platelet activation. Finally, patients with a history of vaso-occlusive crises presented a trend toward increased PDPN expression in monocytes (P = .06). Conclusion: Our findings suggest that the PDPN/CLEC-2 pathway may play an important role in the pathogenesis of thromboinflammation in SCD, especially in patients with the SS genotype. (AU) | |
| Processo FAPESP: | 16/14172-6 - Investigação de aspectos fisiopatológicos e novas abordagens terapêuticas em doenças tromboembólicas |
| Beneficiário: | Joyce Maria Annichino-Bizzacchi |
| Modalidade de apoio: | Auxílio à Pesquisa - Temático |
| Processo FAPESP: | 20/05985-9 - Avaliação dos mecanismos da ativação da hemostasia em COVID-19 e sua modulação por inibidores de bradicinina |
| Beneficiário: | Erich Vinicius de Paula |
| Modalidade de apoio: | Auxílio à Pesquisa - Regular |
| Processo FAPESP: | 19/18886-1 - Mecanismos fisiopatológicos e tratamento das anormalidades das células vermelhas do sangue |
| Beneficiário: | Fernando Ferreira Costa |
| Modalidade de apoio: | Auxílio à Pesquisa - Temático |
| Processo FAPESP: | 22/13216-0 - Interação entre hemostasia e imunidade inata (Imunotrombose): caracterização e exploração fisiopatológica, diagnóstica e terapêutica em doenças infecciosas e inflamatórias |
| Beneficiário: | Erich Vinicius de Paula |
| Modalidade de apoio: | Auxílio à Pesquisa - Temático |
| Processo FAPESP: | 23/08178-5 - O papel da via podoplanina e CLEC-2 na doença falciforme |
| Beneficiário: | Ivanio Teixeira de Borba Junior |
| Modalidade de apoio: | Bolsas no Brasil - Doutorado |