An endothelial proinflammatory phenotype precedes the development of the engraftment syndrome after autologous Hct

Engraftment syndrome (ES) is a common complication after autologous hematopoietic cell transplantation (auto-HCT) whose pathophysiological substrate remains unclear. We investigated whether endothelial damage could contribute to ES. Circulating ECs-damage biomarkers were measured in plasma from pati...

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Published in:Bone marrow transplantation (Basingstoke) 2022-05, Vol.57 (5), p.721-728
Main Authors: Moreno-Castaño, Ana Belén, Palomo, Marta, Torramadé-Moix, Sergi, Martinez-Sanchez, Julia, Ramos, Alex, Molina, Patricia, Pino, Marc, Gómez-Ramírez, Pilar, Bonastre, Laura, Solano, Maria Teresa, Escolar, Ginés, Rovira, Montserrat, Rodríguez-Lobato, Luis Gerardo, Gutiérrez-García, Gonzalo, Carreras, Enric, Fernández-Avilés, Francesc, Diaz-Ricart, Maribel
Format: Article
Language:English
Subjects:
Autografts
Biomarkers
Biomarkers - metabolism
Cadherins
Cell activation
Damage
Endothelial cells
Endothelial Cells - metabolism
Exposure
Hematologic Diseases
Hematopoietic Stem Cell Transplantation - adverse effects
Humans
Immune System Diseases
Inflammation
Intercellular Adhesion Molecule-1
Intracellular signalling
Leukocytes
Phenotype
Phenotypes
Phosphorylation
Proteins
Stem cell transplantation
Substrates
Transplantation
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Summary:Engraftment syndrome (ES) is a common complication after autologous hematopoietic cell transplantation (auto-HCT) whose pathophysiological substrate remains unclear. We investigated whether endothelial damage could contribute to ES. Circulating ECs-damage biomarkers were measured in plasma from patients with (ES; n = 14) or without ES (non-ES; n = 20), collected at different time points: before HCT, 5 (S5) and 10 days (S10) after HCT, and at either the ES onset (SON) or the discharge day (SDIS). Also, cultured endothelial cells (ECs) were exposed to serum samples, obtained at the same points, to evaluate changes in ECs-activation (ICAM-1, VE-Cadherin) biomarkers, the reactivity of ECs towards leukocytes, and activation of intracellular signaling proteins related to inflammation (p38MAPK) and proliferation (Erk1/2). Results showed that circulating VWF, sTNFR1 and sVCAM-1 levels were higher in ES patients at all the points assessed, especially at SON. In vitro results showed an increased ICAM-1 expression on ECs exposed to ES samples vs. non-ES samples, especially to S5, with elevated leukocyte adhesion. Also, a lower VE-Cadherin expression and an increased phosphorylation of p38MAPK and Erk1/2 proteins were observed in ECs exposed to ES vs. non-ES samples. Our results indicate that endothelial activation precedes ES development and could be one of its pathophysiological substrates.
ISSN:0268-3369
1476-5365
DOI:10.1038/s41409-022-01610-z