학술논문
Nrf2 Null Mice Are Deficient in CD169+Macrophages, Associated with Impaired Erythroid Response and Delayed Recovery from Acute Blood Loss
Document Type
Article
Author
Source
Blood; November 2019, Vol. 134 Issue: 1, Number 1 Supplement 1 p1038-1038, 1p
Subject
Language
ISSN
00064971; 15280020
Abstract
Erythropoiesis occurs in specialized niches in the bone marrow consisting of a central macrophage, surrounded by differentiating erythroblasts. This central macrophage has been identified by several markers including, CD169 (Sialoadhesin or Siglec-1), F4/80, CD11b, VCAM-1, ER-HR3 and Ly-6G. These CD169+macrophages support erythropoiesis both at steady state and during stress. Nuclear factor erythroid 2-related factor 2 (Nrf2) is the master regulator of the cellular oxidative defense system. It modulates hematopoietic stem cells but its loss produces no visible phenotype in steady state hematological parameters. However, the importance of Nrf2 and macrophage subsets has not been fully characterized during recovery from stress erythropoiesis. We examined specific subsets of CD169+macrophage populations in Nrf2 knockout (Nrf2−/−) mice as well as the role of Nrf2 in recovery from stress erythropoiesis in vivo.