Dataset Information

Expression data from Aortic Macrophages

ABSTRACT: Normal arteries contain a large population of tissue resident macrophages (MΦ). Their origins, as well as the mechanisms that sustain them during homeostasis and disease, however, are poorly understood. Gene expression profiling, we show, identifies arterial MΦ as a distinct population among tissue MΦ. Ontologically, arterial MΦ arise before birth, though CX3CR1-, Csf1r-, and Flt3-driven fate mapping approaches demonstrate MΦ colonization occurs through successive contributions of yolk sac (YS) and conventional hematopoiesis. In adulthood, arterial MΦ renewal is driven by local proliferation rather than monocyte recruitment from the blood. Proliferation sustains MΦ not only during steady state conditions, but mediates their rebound after severe depletion following sepsis. Importantly, the return of arterial MΦ to functional homeostasis after infection is rapid; repopulated MΦ exhibit a transcriptional program similar to resting MΦ and efficiently phagocytose bacteria. Collectively, our data provide a detailed framework for future studies of arterial MΦ function in health and disease.

ORGANISM(S): Mus musculus

PROVIDER: GSE68968 | GEO | 2015/12/07

SECONDARY ACCESSION(S): PRJNA284232

REPOSITORIES: GEO

ACCESS DATA

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Project description:Background：Atherosclerosis is the major cause of cardiovascular disease. Endothelial injury is one of the initiating factors of atherosclerosis. Injured endothelial cells overexpress adhesion molecules such as vascular cell adhesion molecule-1 (VCAM-1) and intercellular adhesion molecule-1 (ICAM-1), facilitating the binding and accumulation of monocytes-macrophages into the vascular wall via the ligands. Adipose-derived stem cells (ADSCs) have been extensively researched for their anti-inflammatory properties and therapeutic potential in various diseases. Targeting atherosclerotic regions with ADSCs may offer a promising therapeutic strategy to alleviate local inflammation associated with atherosclerosis.Methods：The ligands of very late antigen-4 (VLA-4) and lymphocyte function-associated antigen-1 (LFA-1) were expressed in the ADSC to construct the Macrophage (Mφ)-mimicking ADSCs. Cell proliferation, adhesion, and migration assays were used to characterize the Mφ-mimicking ADSCs. An atherosclerosis model was established in ApoE-/- mice via partial carotid artery ligation. Mφ-mimicking ADSCs were administered through tail vein injection. Distribution of these cells was tracked by far-red fluorescent probe. Histological analyses, including H&E staining, Oil Red O staining, and immunofluorescence were conducted to assess the impact on plaque size, composition, and macrophage polarization.Results：Mφ-mimicking ADSCs were successfully constructed and characterized. These cells exhibited enhanced adhesion and migration capabilities. The culture medium from Mφ-mimicking ADSCs increased the proportion of M2 macrophages and decreased the lipid uptake capacity. In the atherosclerosis mouse model, fluorescently labeled Mφ-mimicking ADSCs specifically adhered to and accumulated in atherosclerotic regions, demonstrating targeted localization. Mφ-mimicking ADSC treatment resulted in a reduction in plaque size and a decrease in the number of M1 macrophages within the arterial wall.Conclusions：Mφ-mimicking ADSCs confirmed their preserved anti-inflammatory properties and enhanced adhesion and migration abilities. In vivo, Mφ-mimicking ADSCs exhibited targeted localization ability to regions of endothelial dysfunction in atherosclerosis and attenuate plaque progression. These findings suggest that Mφ-mimicking ADSCs may serve as a potential therapeutic strategy for alleviating atherosclerosis and reducing inflammation.

Dataset Information

Expression data from Aortic Macrophages

Dataset's files

Similar Datasets

OmicsDI is part of the ELIXIR infrastructure

Tweets