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Id1 and Id3 Maintain Steady-State Hematopoiesis by Promoting Sinusoidal Endothelial Cell Survival and Regeneration.

Abstract：

:Investigating mechanisms that regulate endothelial cell (EC) growth and survival is important for understanding EC homeostasis and how ECs maintain stem cell niches. We report here that targeted loss of Id genes in adult ECs results in dilated, leaky sinusoids and a pro-inflammatory state that increases in severity over time. Disruption in sinusoidal integrity leads to increased hematopoietic stem cell (HSC) proliferation, differentiation, migration, and exhaustion. Mechanistically, sinusoidal ECs (SECs) show increased apoptosis because of reduced Bcl2-family gene expression following Id gene ablation. Furthermore, Id1-/-Id3-/- SECs and upstream type H vessels show increased expression of cyclin-dependent kinase inhibitors p21 and p27 and impaired ability to proliferate, which is rescued by reducing E2-2 expression. Id1-/-Id3-/- mice do not survive sublethal irradiation because of impaired vessel regeneration and hematopoietic failure. Thus, Id genes are required for the survival and regeneration of BM SECs during homeostasis and stress to maintain HSC development.

journal_name

Cell Rep

journal_title

Cell reports

authors

Gadomski S,Singh SK,Singh S,Sarkar T,Klarmann KD,Berenschot M,Seaman S,Jakubison B,Gudmundsson KO,Lockett S,Keller JR

doi

10.1016/j.celrep.2020.107572

subject

Has Abstract

pub_date

2020-04-28 00:00:00

pages

107572

issue

4

issn

2211-1247

pii

S2211-1247(20)30521-0

journal_volume

31

pub_type

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