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Retrospective analysis reveals the early origin and development of pulmonary perivascular cells [MeD-seq]

ABSTRACT: Emerging evidence suggests pericytes play a significant role in various lung diseases. However, characterizing pericytes remains challenging, impeding our understanding of their role in lung development and disease. Using single-cell RNA sequencing and DCM-time machine technology, we tracked the development of mouse pulmonary pericytes. Our study revealed the differentiation of perivascular progenitors into pericytes and vascular smooth muscle cells. Temporal analysis uncovered dynamic gene expression profiles during pericyte differentiation, highlighting pathways crucial for pulmonary vascular development. Further analysis showed intricate signaling interactions between pericyte progenitors and mature pericytes, and we validated Mcam as a bona fide pulmonary pericyte marker. These findings challenge conventional views on pericyte origin and underscore the importance of accurate pericyte identification in developmental and disease contexts. Overall, this study enhances our understanding of pulmonary pericyte ontogeny and differentiation, offering insights into their potential as therapeutic targets in pericyte-associated lung diseases.

ORGANISM(S): Mus musculus

PROVIDER: GSE268412 | GEO | 2026/03/23

REPOSITORIES: GEO

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Retrospective analysis reveals the early origin and development of pulmonary perivascular cells [scRNA-seq]

Project description:Emerging evidence suggests pericytes play a significant role in various lung diseases. However, characterizing pericytes remains challenging, impeding our understanding of their role in lung development and disease. Using single-cell RNA sequencing and DCM-time machine technology, we tracked the development of mouse pulmonary pericytes. Our study revealed the differentiation of perivascular progenitors into pericytes and vascular smooth muscle cells. Temporal analysis uncovered dynamic gene expression profiles during pericyte differentiation, highlighting pathways crucial for pulmonary vascular development. Further analysis showed intricate signaling interactions between pericyte progenitors and mature pericytes, and we validated Mcam as a bona fide pulmonary pericyte marker. These findings challenge conventional views on pericyte origin and underscore the importance of accurate pericyte identification in developmental and disease contexts. Overall, this study enhances our understanding of pulmonary pericyte ontogeny and differentiation, offering insights into their potential as therapeutic targets in pericyte-associated lung diseases.

2026-03-23 | GSE268413 | GEO

FOXF2 regulates pericyte function required for pericyte-endothelial signaling during neonatal hyperoxic lung injury [scRNA-seq]

Project description:Pulmonary vascular development is essential for alveolarization, and disruption of this process contributes to bronchopulmonary dysplasia (BPD) pulmonary pathology. Proper vascular development requires an orchestration of many cell types within the lung. However, the mechanisms by which pericytes support the endothelium in the postnatal lung remain poorly understood. Here, we identify FOXF2 as a critical transcription factor that governs pericyte maturation and function during postnatal lung development and regeneration. FOXF2 expression in pericytes increases postnatally and is selectively downregulated following neonatal hyperoxic injury. Pdgfrb-CreER mediated Foxf2 deletion in pericytes leads to pericyte hyperplasia, impaired migration, reduced expression of angiogenic factors such as ANGPTL4, and exacerbated alveolar simplification in a neonatal murine model of BPD. Transcriptomic and genomic studies demonstrate that FOXF2 maintains chromatin accessibility at pro-angiogenic loci and modulates paracrine signaling essential for endothelial regeneration. Loss of FOXF2 disrupts pericyte–endothelial crosstalk, impairing angiogenesis and alveolar repair during injury. Our study identifies FOXF2 as a central transcriptional regulator of pericyte-driven vascular niche function in the neonatal lung and underscores the pathogenic role of dysfunctional pericytes in BPD.

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FOXF2 regulates pericyte function required for pericyte-endothelial signaling during neonatal hyperoxic lung injury [RNA-Seq]

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Project description:Vascular remodeling is the process of structural alteration and cell rearrangement of blood vessels in response to injury and is the cause of many of the world's most afflicted cardiovascular conditions, including pulmonary arterial hypertension(PAH). Many studies have focused on the effects of vascular endothelial cells and smooth muscle cells(SMCs) during vascular remodeling, but pericytes, an indispensable cell population residing largely in capillaries, are ignored in this maladaptive process. Here we report that hypoxia-inducible factor 2α(HIF2α) expression is increased in human PAH patient lung tissues and HIF2α overexpressed pericytes result in greater contractility and an impaired endothelial-pericyte interaction. Using single-cell RNAseq and hypoxia-induced pulmonary hypertension(PH) models, we show HIF2α as a major molecular regulator for pericytes’ transformation into SMC-like cells. HIF2α overexpression in pericyte-selective mice exacerbate PH and right ventricular hypertrophy. Temporal cellular lineage tracing shows that HIF2α overexpressing reporter NG2+ cells (pericyte-selective) relocate from capillaries to arterioles and co-express SMA. This novel insight into the potential role of NG2+ pericytes in pulmonary vascular remodeling via HIF2α signaling suggests a potential drug target for PH.

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Pericytes contribute to pulmonary vascular remodeling via HIF2α signaling

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

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