Endothelial damage and a thin intercellular fibrin network promote haemorrhage in acute promyelocytic leukaemia.

ABSTRACT:

Background

The role of vascular endothelium in acute promyelocytic leukaemia (APL) remains unknown. We aimed to investigate the mechanisms by which APL cells interact with endothelial cells (ECs) and to further explore how the endothelium affects bleeding as well as therapeutic interventions.

Method

APL cells and an original APL cell line, NB4 cells, were used for experiments. The effects of leukaemic cells on ECs were analyzed in vitro and in vivo. Moreover, the endothelial barrier function and procoagulant activity were detected. An APL mouse model was established for in vivo studies.

Findings

APL cells interacted with ECs via ICAM-1 and VCAM-1 receptors to disrupt endothelial integrity. This binding activated MLCK signaling, resulting in the trans-endothelial passa

SUBMITTER: Wang C 

PROVIDER: S-EPMC7501057 | biostudies-literature | 2020 Oct

REPOSITORIES: biostudies-literature