Data set related to the article: "SARS-CoV-2 Lysate Stimulation Impairs the Release of Platelet-like Particles and Megakaryopoiesis in the MEG-01 Cell Line."
Authors/Creators
- 1. Department of Medicine, Surgery and Dentistry "Scuola Medica Salernitana", University of Salerno, Via Salvatore Allende, 84081 Baronissi, Italy
- 2. Department of Experimental Medicine, University of Campania "Luigi Vanvitelli", 80138 Naples, Ital
- 3. Department of Medicine, Surgery and Dentistry "Scuola Medica Salernitana", University of Salerno, Via Salvatore Allende, 84081 Baronissi, Italy Department of Experimental Medicine, University of Campania "Luigi Vanvitelli", 80138 Naples, Italy
- 4. Department of Medicine, Surgery and Dentistry "Scuola Medica Salernitana", University of Salerno, Via Salvatore Allende, 84081 Baronissi, Italy; Cardiovascular Research Unit, IRCCS MultiMedica, 20138 Milan, Italy
Description
Abstract:
SARS-CoV-2 infection causes a considerable inflammatory response coupled with impaired platelet reactivity, which can lead to platelet disorders recognized as negative prognostic factors in COVID-19 patients. The virus may cause thrombocytopenia or thrombocytosis during the different disease stages by destroying or activating platelets and influencing platelet production. While it is known that several viruses can impair megakaryopoiesis by generating an improper production and activation of platelets, the potential involvement of SARS-CoV-2 in affecting megakaryopoiesis is poorly understood. To this purpose, we explored, in vitro, the impact of SARS-CoV-2 stimulation in the MEG-01 cell line, a human megakaryoblastic leukemia cell line, considering its spontaneous capacity of releasing platelet-like particles (PLPs). We interrogated the effect of heat-inactivated SARS- CoV-2 lysate in the release of PLPs and activation from MEG-01, the signaling pathway influenced by SARS-CoV-2, and the functional effect on macrophagic skewing. The results highlight the potential influence of SARS-CoV-2 in the early stages of megakaryopoiesis by enhancing the production and activation of platelets, very likely due to the impairment of STATs signaling and AMPK activity. Overall, these findings provide new insight into the role of SARS-CoV-2 in affecting megakaryocyte– platelet compartment, possibly unlocking another avenue by which SARS-CoV-2 moves.