Platelets from mice lacking the aryl hydrocarbon receptor exhibit defective collagen-dependent signaling.

ABSTRACT:

Background

We previously identified aryl hydrocarbon receptor (AHR) as a novel regulator of megakaryocytic differentiation and polyploidization and reported that AHR-null mice have approximately 15% fewer platelets than do wild-type mice, yet they exhibit a dramatic, unexplained bleeding phenotype.

Objectives

The current work tests our hypothesis that AHR-null platelets are functionally deficient, contributing to the previously reported (yet unexplained) bleeding phenotype present in AHR-null mice.

Methods

AHR-null bone marrow was ex vivo differentiated with thrombopoietin with or without AHR ligands or AHR inhibitors and analyzed for degree of megakaryopoiesis and polyploidization. Platelet function of AHR-null mice was assessed with aggregation and spreading assays.

SUBMITTER: Lindsey S 

PROVIDER: S-EPMC4008149 | biostudies-literature | 2014

REPOSITORIES: biostudies-literature