C-MAF defines the phenotype of a family of perivascular macrophages
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ABSTRACT:
PROVIDER: PRJNA625192 | ENA |
REPOSITORIES: ENA
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Project description:Tissue-resident Macrophages have long been appreciated as playing a fundamental role in the ontogeny and function of several organs. For example, osteoclasts are crucial for proper bone remodeling, microglia for synaptic pruning, and lung alveolar macrophages for clearance of surfactant. Perivascular macrophages have been described in many organs. Our analysis of murine perivascular macrophages in several tissues and organs led us to define a macrophage family, whose members share the expression of a number of surface molecules that are not typically considered macrophage markers, such as Lyve1, Folate Receptor 2 (Folr2), Enpep/CD249, and CD38, as well as other more typical macrophage markers such as CD206 and Tim4. This family of perivascular macrophages also occurs in humans. Importantly, this family of perivascular macrophages relies on the transcription factor c-MAF, encoded by the gene Maf, for its full function. Conditional deletion of the Maf gene in the Lyve1+Folr2+CD38+ macrophage family caused their ablation in the brain, without impact on the microglia, while in the adipose tissue the conditional deletion of the Maf gene in perivascular macrophages resulted in a profoundly altered macrophage gene expression, and brought about an increased vascular branching in this tissue. Mice with conditional Maf deletion were protected from metabolic syndrome when submitted to high fat diet (HFD). Our results show that c-MAF is the master regulator of a family of perivascular macrophages.
2021-09-30 | GSE148606 | GEO
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2019-12-16 | PXD016020 | Pride
Project description:Inflammatory crosstalk between perivascular adipose tissue and and blood vessel wall may contribute to atherosclerosis pathogenesis, and exhibits more pro-inflammatory than adipogenic phenotype than subcutaneous adipocytes. To identify a genomic basis for biologic differences, we performed genome-wide expression to identiy expression genes differentially regulated between perivascular and subcutaneous adipocytes.for biologic differences. We performed global gene expression analyses on in vitro differentiated adipocytes from human left coronary artery perivascular adipose tissue and subcutaneous adipose tissues derived from unrelated donors who were non-obese and did not have any known metabolic or atherosclerotic disease.
2013-03-15 | E-GEOD-45169 | biostudies-arrayexpress
Project description:A population of endometrial cells displaying key properties of mesenchymal stem cells (eMSC) has been identified in human endometrium. eMSC co-express CD146 and PDGFRB surface markers, have a perivascular location, and likely represent the reservoir of progenitors giving rise to the endometrial stromal fibroblast lineage. Endometrial stromal cells isolated from 16 oocyte donors and 3 benign gynecologic surgery subjects were FACS sorted into four populations: CD146+/PDGFRB+ (eMSC); CD146+/PDGFRB- (endothelial cells); CD146-/PDGFRB+ (stromal fibroblasts); CD146-/PDGFRB- (mixed population) then subjected to gene expression analysis on Affymetrix Human Gene 1.0 ST arrays, and differentially expressed genes compared between eMSC, stromal fibroblast, and endothelial cell populations. Ninety-two genes were validated by multiplex quantitative RT-PCR on seventy of these sorted cell populations. Immunohistochemistry was used to verify the perivascular location of eMSCs.Principal component analysis and hierarchical clustering showed eMSC clustering discretely near stromal fibroblasts and separately from endothelial cells. eMSC expressed pericyte markers and genes involved hypoxia response, inflammation, proteolysis, and angiogenesis/vasculogenesis – all relevant to endometrial tissue breakdown and regeneration. Additionally, eMSC displayed distinct gene profiles for cell-cell communication and regulation of gene expression. Overall, the phenotype of the eMSC is that of a multipotent pericyte responsive to hypoxic, proteolytic, and inflammatory stimuli, able to induce angiogenesis, migrate and differentiate into lineage cells, and potentially respond to estradiol and progesterone. Identifying the pathways and gene families described herein in the context of the endometrial niche, will be valuable in understanding normal and abnormal endometrial development in utero and differentiation in adult uterus. The multipotent, perivascular endometrial mesenchymal stem cell has a “niche phenotype” of high Notch, TGFB, IGF, and Hedgehog and low canonical/non-canonical Wnt and EGF signaling. Oocyte donors with no known uterine pathology underwent endometrial biopsy at the time of oocyte retrieval, following comparable GnHR agonist downregulated ovarian stimulation protocols. Tissue was digested and stromal cells isolated and sorted based on expression of CD146 and PDGFRB. RNA was extracted and hybridized on Affymetrix microarrays. Resulting data were compared between sorted isolated cell populations.
2011-11-14 | E-GEOD-31152 | biostudies-arrayexpress
Project description:Homozygous disruption of c-Maf led to embryonic lethality and impaired erythroblastic island formation. c-Maf is expressed in the fetal liver macrophages. It suggests that macrophages are responsible for the lethality of c-Maf knock-out embryos. To search downstream genes of c-Maf, we surveyed genes associated with macrophage function by microarray analysis. keywords: c-Maf, macrophage, erythroblastic islands, WT (c-Maf WT) and c-Maf KO (c-Maf KO) fetal liver macrophages were sorted by a FACSAria cell sorter. Total RNAs from those macrophages were prepared using RNeasy Kit. Genes down-regulated in c-Maf KO macrophages were searched by GeneSpring software.
2011-07-06 | E-GEOD-23305 | biostudies-arrayexpress
Project description:To investigate the function of Maf family transcription factors, MafB and cMaf, in the intestinal epithelium, we generated tissue specific loss of function mouse models.
2022-10-14 | GSE208763 | GEO
Project description:Transcription factor Maf-S knockdown by dsRNA injection and compared to dsRNA-GFP injected control. Maf-S knockdown was performed to study the affect of xenobiotic stress of the cnc-keap1 pathway.
2017-03-19 | E-MTAB-4042 | biostudies-arrayexpress
Project description:Aim of this experiment was to characterize whether SPP1 released from the hippocampal perivascular space could imprint microglia transcriptional states. We performed scRNA-seq analysis on sorted CD140a+ perivascular fibroblast (PVF), CD45highCD11intCD206+ perivascular macrophage (PVM) and CD45intCD11intCX3CR1high microglial cell from dissected hippocampi of 6-month old wild type vs SPP1KO/KO vs AppNL-F mice vs AppNL-FxSpp1KO/KO mice. Cells were isolated from dissected hippocampi as previously described (Sala Frigerio et al.,2019).
2024-02-09 | E-MTAB-11918 | biostudies-arrayexpress
Project description:Inflammatory crosstalk between perivascular adipose tissue and and blood vessel wall may contribute to atherosclerosis pathogenesis, and exhibits more pro-inflammatory than adipogenic phenotype than subcutaneous adipocytes. To identify a genomic basis for biologic differences, we performed genome-wide expression to identiy expression genes differentially regulated between perivascular and subcutaneous adipocytes.for biologic differences.
2013-03-15 | GSE45169 | GEO
Project description:Background: Melanoma brain metastases (MBM) continues to be a significant clinical problem with limited treatment options. Highly invasive melanoma cells migrate along the vasculature and perivascular cells may contribute to residual disease and recurrence. PTEN loss and hyperactivation of AKT occur in MBM; however, a role for PTEN/AKT in perivascular invasion has not been described. Methods: We used in vivo intracranial injections of murine melanoma and bulk RNA sequencing of melanoma cells co-cultured with brain endothelial cells (brECs) to investigate brain colonization and perivascular invasion. Results: We found that PTEN-null melanoma cells were highly efficient at colonizing the perivascular niche relative to PTEN-expressing counterparts. PTEN re-expression (PTEN-RE) in melanoma significantly reduced brain colonization and migration along the vasculature. We hypothesized this phenotype was mediated through vascular-induced TGFβ secretion, which drives AKT phosphorylation. Disabling TGFβ signaling in melanoma cells reduced colonization and perivascular invasion; however, introduction of constitutively-active myristolated-AKT (myrAKT) restored overall tumor size but not perivascular invasion. Conclusions: PTEN loss facilitates perivascular brain colonization and invasion of melanoma. TGFβ-AKT signaling partially contributes to this phenotype, but further studies are needed to determine the complementary mechanisms that enable melanoma cells to both survive and spread along the brain vasculature.
2023-12-26 | GSE247232 | GEO