Objective: To investigate the effect and mechanism of Factor Xa on the differentiation of Meg-01 cells into platelet-like particles.
Methods: The Meg-01 cells were used as experimental object, Factor Xa was used as agonist. Cell proliferation was detected by CCK-8 assay. The viability of platelet-like particles was analyzed by AlamaBlue kit. MAPK/ERK pathway and PI3K/AKT pathway were assayed by Western blot. The expression of CD41b was analyzed by Western blot and flow cytometry. Cell cycle and apoptosis were detected by flow cytometry.
Results: The Factor Xa (1 µg/ml) inhibited cell viability, induced apoptosis. Factor Xa triggered cell arrest at the G(2)/M stage and down-regulated the expression of SKP2. After Meg-01 cells were stimulated by Factor Xa, the expression of CD41b was up-regulated and the MAPK/ERK pathway and PI3K/AKT pathway were activated. The platelets-like particles stimulated by FXa activation were viable.
Conclusion: The Factor Xa maybe display some effect on the differentiation of megakaryocytes into platelets.
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http://dx.doi.org/10.7534/j.issn.1009-2137.2016.02.040 | DOI Listing |
Platelets
December 2025
Department of Pharmacology and Physiology, George Washington University, Washington, DC, USA.
Platelet-like particles (PLPs), derived from megakaryocytic cell lines MEG-01 and K-562, are widely used as a surrogate to study platelet formation and function. We demonstrate by RNA-Seq that PLPs are transcriptionally distinct from platelets. Expression of key genes in signaling pathways promoting platelet activation/aggregation, such as the PI3K/AKT, protein kinase A, phospholipase C, and α-adrenergic and GP6 receptor pathways, was missing or under-expressed in PLPs.
View Article and Find Full Text PDFBiomolecules
October 2024
College of Pharmacy, Kyungsung University, 309 Suyeong-ro, Busan 48434, Republic of Korea.
Platelets are essential blood components that maintain hemostasis, prevent excessive bleeding, and facilitate wound healing. Reduced platelet counts are implicated in various diseases, including leukemia, hepatitis, cancer, and Alzheimer's disease. Enhancing megakaryocytic differentiation is a promising strategy to increase platelet production.
View Article and Find Full Text PDFThromb Res
December 2024
Faculty of Pharmacy and Pharmaceutical Sciences, University of Alberta, Edmonton, Canada; Department of Pharmacology, Faculty of Medicine and Dentistry, University of Alberta, Edmonton, Canada; Cardiovascular Research Institute, University of Alberta, Edmonton, AB, Canada; Cancer Research Institute of Northern Alberta, University of Alberta, Edmonton, AB, Canada. Electronic address:
Background: Platelet-rich microvascular thrombi are common in severe COVID-19. Endogenous nitric oxide (NO)-signaling limits thrombus formation and previously we identified platelet subpopulations with a differential ability to produce NO based on the presence or absence of endothelial nitric oxide synthase (eNOS). eNOS expression is counter-regulated by cytokines, and COVID-19-associated immune/inflammatory responses may affect the transcriptome profile of megakaryocytes and their platelet progeny.
View Article and Find Full Text PDFJ Mol Cell Biol
October 2024
Centre d'Infection et d'Immunité de Lille, INSERM U1019, CNRS UMR9017, Institut Pasteur de Lille, Lille 59019, France.
Despite an undetectable plasma viral load as a result of antiretroviral therapy, HIV-1-infected individuals with poor immune reconstitution harbor infectious HIV-1 within their platelets. Megakaryocytes, as platelet precursors, are the likely cellular origin of these HIV-1-containing platelets. To investigate the mechanisms that allow megakaryocytes to support HIV-1 infection, we established in vitro models of viral infection using hematopoietic stem cell-derived megakaryocytes and the megakaryocytic MEG-01 cell line.
View Article and Find Full Text PDFHeliyon
August 2024
Department of Transfusion Medicine, Huashan Hospital, Fudan University, Shanghai, 200040, China.
Background: Type 2 diabetes mellitus (T2DM) presents a thrombotic environment, contributing to diabetic macroangiopathy and microangiopathy. In this study, the regulation of microthrombosis in T2DM was assessed.
Methods: Platelets from T2DM patients and healthy controls were analyzed using 4D label-free proteomics and bioinformatics.
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