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Single-cell RNA sequencing of hyaloid blood vessels from endothelial-specific Gpr124 knockout mice and control littermates

ABSTRACT: To explore the molecular mechanisms of GPR124-mediated hyaloid blood vessel regression, single-cell RNA sequencing of hyaloid vessels from P6 endothelial-specific Gpr124 knockout mice and control littermates was performed. The sequenced cells clustered into two major populations: endothelial cells and pericytes. Differential gene expression analysis suggested that GPR124 regulates WNT/β-catenin signaling in hyaloid endothelial cells and mediates partial endothelial-mesenchymal transition (EndMT).

ORGANISM(S): Mus musculus

PROVIDER: GSE284257 | GEO | 2026/04/27

REPOSITORIES: GEO

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CD44+ Lung Cancer Stem Cell-derived Vascular Pericytes Cause Brain Metastases through GPR124-mediated Trans-endothelial Migration [II]

Project description:Brain metastasis of lung cancer causes high mortality, but the exact mechanisms underlying the metastasis remain unclear. Here we report that vascular pericytes derived from CD44+ lung cancer stem cells (CSCs) in lung adenocarcinoma (ADC) potently cause brain metastases through GPR124-mediated trans-endothelial migration (TEM). CD44+ CSCs in the perivascular niche generate the majority of vascular pericytes in lung ADC. CSC-derived pericyte-like cells (Cd-pericytes) exhibit remarkable TEM capacity to effectively intravasate into vessel lumina, survive in the circulation, extravasate into the brain parenchyma, and then de-differentiate into tumorigenic CSCs to form metastases. Moreover, Cd-pericytes uniquely express GPR124, a G-protein-coupled receptor. GPR124 mediates through Wnt7-β-Catenin activation to enhance TEM capacity of Cd-pericytes for intravasation and extravasation, two critical steps during tumor metastasis. Furthermore, selective disruption of Cd-pericytes, GPR124 or Wnt7-β-Catenin signaling markedly reduced brain and liver metastases of lung ADC. Our findings uncover an unappreciated cellular and molecular paradigm driving tumor metastasis.

2023-07-23 | GSE237317 | GEO

CD44+ Lung Cancer Stem Cell-derived Vascular Pericytes Cause Brain Metastases through GPR124-mediated Trans-endothelial Migration [I]

2023-07-23 | GSE237316 | GEO

Single-cell RNA sequencing of hyaloid blood vessels from endothelial-specific Gpr124 knockout mice and control littermates

Project description:Single-cell RNA sequencing of hyaloid blood vessels from endothelial-specific Gpr124 knockout mice and control littermates

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Gpr124 is essential for blood-brain barrier integrity in central nervous system disease

Project description:Although blood-brain barrier (BBB) compromise is central to the etiology of diverse central nervous system (CNS) disorders, endothelial receptor proteins that control BBB function are poorly defined. The endothelial G protein-coupled receptor (GPCR) Gpr124 has been reported to be required for normal forebrain angiogenesis and BBB function in mouse embryos, but the role of this receptor in adults is unknown. Here, conditional Gpr124 knockout (CKO) in the endothelia of adult mice did not affect homeostatic BBB integrity but resulted in BBB disruption and microvascular hemorrhage in mouse models of ischemic stroke and glioblastoma, accompanied by reduced cerebrovascular canonical Wnt/beta-catenin signaling. Constitutive activation of Wnt/beta-catenin signaling fully corrected the BBB disruption and hemorrhage defects of Gpr124 cko mice, with rescue of the endothelial tight junction, pericyte coverage and extracellular-matrix deficits. We thus identify Gpr124 as an endothelial GPCR specifically required for endothelial Wnt signaling and BBB integrity under pathological conditions in adult mice. This finding implicates Gpr124 as a potential therapeutic target for human CNS disorders characterized by BBB disruption.

2017-03-06 | GSE74052 | GEO

GPR124 regulates murine CNS angiogenesis and blood-brain barrier formation by an intracellular domain-independent mechanism

Project description:The GPR124/RECK/WNT7 pathway essentially regulates central nervous system angiogenesis and blood-brain barrier (BBB) function. GPR124, a brain endothelial adhesion 7-pass transmembrane protein, associates with membrane RECK, which binds and stabilizes newly synthesized WNT7 for subsequent transfer to Frizzled (FZD) and canonical b-catenin signaling. GPR124 function remains enigmatic; while its extracellular domain (ECD) is required, the poorly conserved intracellular domain (ICD) appears to be variably required in mammals versus zebrafish, potentially mediated by bridging of the GPR124 and FZD ICDs by intracellular adaptor proteins. GPR124 ICD deletion mutants impair zebrafish angiogenesis, but paradoxically still mediate WNT7 signaling upon mammalian cell transfection. We thus further investigated the GPR124 C-terminal ICD by deletion in mice (Gpr124ΔC). Notably, Gpr124ΔC/ΔC mice could be born and did not recapitulate Gpr124-/- embryonic lethal forebrain hemorrhage. GPR124ΔC protein was inefficiently expressed, resulting in mild, hypomorphic, non-hemorrhagic defects in CNS angiogenesis and BBB function, sparing the cortex and only confined to ganglionic eminences. Impaired surface expression of GPR124ΔC directly correlated with reduced endothelial WNT signaling, arguing against an intrinsic signaling deficiency. Further, GPR124ΔC and recombinant GPR124 ECD both rescued WNT7 signaling following brain endothelial Gpr124 knockdown. Thus, in mice, the GPR124 essential regulation of WNT7-dependent CNS forebrain angiogenesis and BBB function is exerted by ICD-independent functionality, extending the range of signaling mechanisms used by adhesion 7-pass transmembrane receptors.

2024-04-19 | GSE225367 | GEO

GPR124 Protects against Podocyte Senescence and Injury in Diabetic Kidney Disease

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Single-Cell Characterization of the Frizzled 5 (Fz5) Mutant Mouse and Human Persistent Fetal Vasculature (PFV)

Project description:During early development, a transitory fetal vasculature of the vitreous hyaloid vessels (HV) provides temporary nutrients for the developing lens and retina. HV regresses when the intraretinal vasculature develops to replace its function. Failure in regression of the HV leads to persistent fetal vasculature (PFV), a pathological condition accounting for 4.8% children blindness in the USA. To date, the HV formation and regression as well as the related PFV pathogenesis are largely unknown. In this study, by single-cell RNA sequencing (scRNA-seq) the vitreous cells derived from normal and the Fzd5 mutant mice at two time points, postnatal day 3 (P3) and P6, we collectively defined 10 major cell types, present in both wild type and mutant developing vitreous but with much higher numbers of endothelial cells, macrophages, erythroid-like cells, pericytes, smooth muscle cells, fibroblasts and melanocytes in the P3 mutants. Both mutant and wild type cell types declined to similar sizes at P6 with varied compositions of sub clusters. We further compared gene expression profiles of residual major sub clusters at P6, and showed altered metabolic activities of the mutant cells. Additionally, two macrophage clusters expressed markers for hyalocytes supporting the notion that these cells are of macrophage origin. The melanocytes predominantly existed in the Fzd5 mutants expressing neural crest markers including Pax3 and Sox10, similar to that of choroidal pigment cells. Taken together, these data revealed cell features of normal and pathological hyaloid tissues, which has not been known precedentially.

2023-05-31 | GSE203116 | GEO

CD44+ Lung Cancer Stem Cell-derived Vascular Pericytes Cause Brain Metastases through GPR124-mediated Trans-endothelial Migration

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Project description:CD44+ Lung Cancer Stem Cell-derived Vascular Pericytes Cause Brain Metastases through GPR124-mediated Trans-endothelial Migration [II]

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CD44+ Lung Cancer Stem Cell-derived Vascular Pericytes Cause Brain Metastases through GPR124-mediated Trans-endothelial Migration [I]

Project description:CD44+ Lung Cancer Stem Cell-derived Vascular Pericytes Cause Brain Metastases through GPR124-mediated Trans-endothelial Migration [I]

| PRJNA994565 | ENA

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