Vasculopathy-associated Hyperangiotensinemia Mobilizes Haematopoietic Stem Cells/progenitors Through Endothelial AT₂R and Cytoskeletal Dysregulation

Overview

Journal Nat Commun

Specialty Biology

Date 2015 Jan 10

PMID 25574809

Citations 10

Authors

Kyung Hee Chang

Ramesh C Nayak

Swarnava Roy

Ajay Perumbeti

Ashley M Wellendorf

Katie Y Bezold

Megan Pirman

Sarah E Hill

Joseph Starnes

Anastacia Loberg

Xuan Zhou

Tadashi Inagami

Yi Zheng

Punam Malik

Jose A Cancelas

Affiliations

Soon will be listed here.

Abstract

Patients with organ failure of vascular origin have increased circulating haematopoietic stem cells and progenitors (HSC/P). Plasma levels of angiotensin II (Ang-II), are commonly increased in vasculopathies. Hyperangiotensinemia results in activation of a very distinct Ang-II receptor set, Rho family GTPase members, and actin in bone marrow endothelial cells (BMEC) and HSC/P, which results in decreased membrane integrin activation in both BMEC and HSC/P, and in HSC/P de-adhesion and mobilization. The Ang-II effect can be reversed pharmacologically and genetically by inhibiting Ang-II production or signalling through BMEC AT2R, HSCP Ang-II receptor type 1 (AT1R)/AT2R or HSC/P RhoA, but not by interfering with other vascular tone mediators. Hyperangiotensinemia and high counts of circulating HSC/P seen in sickle cell disease (SCD) as a result of vascular damage, is significantly decreased by Ang-II inhibitors. Our data define for the first time the role of Ang-II HSC/P traffic regulation and redefine the haematopoietic consequences of anti-angiotensin therapy in SCD.

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