[ Disclaimer: This projects/Data has been created for the Gupta lab at Brigham and Women's Hospital (Harvard Medical School) and it's collaborators as an internal reference. All the data has been downloaded from the publicly available data base. Due acknowledgments are given as below. It is not intended for the public release ]
[Article]
JCI Insight. 2019 Feb 21;4(4). pii: 124574. doi: 10.1172/jci.insight.124574. eCollection 2019 Feb 21.
Single-cell analysis of fate-mapped macrophages reveals heterogeneity, including stem-like properties, during atherosclerosis progression and regression.
Lin JD, Nishi H, Poles J, Niu X, Mccauley C, Rahman K, Brown EJ, Yeung ST, Vozhilla N, Weinstock A, Ramsey SA, Fisher EA, Loke P
Abstract
Atherosclerosis is a leading cause of death worldwide in industrialized countries. Disease progression and regression are associated with different activation states of macrophages derived from inflammatory monocytes entering the plaques. The features of monocyte-to-macrophage transition and the full spectrum of macrophage activation states during either plaque progression or regression, however, are incompletely established. Here, we use a combination of single-cell RNA sequencing and genetic fate mapping to profile, for the first time to our knowledge, plaque cells derived from CX3CR1+ precursors in mice during both progression and regression of atherosclerosis. The analyses revealed a spectrum of macrophage activation states with greater complexity than the traditional M1 and M2 polarization states, with progression associated with differentiation of CXC3R1+ monocytes into more distinct states than during regression. We also identified an unexpected cluster of proliferating monocytes with a stem cell-like signature, suggesting that monocytes may persist in a proliferating self-renewal state in inflamed tissue, rather than differentiating immediately into macrophages after entering the tissue.
KEYWORDS: Atherosclerosis; Cardiology; Immunology; Macrophages; Molecular diagnosis
CAUTION: Please do not make the data to public!.
PMID: 30830865 PMCID: PMC6478411 DOI: 10.1172/jci.insight.124574
Data: GSE123587
