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Advancing Lung Tissue Engineering Through the Discovery of Factors that Control Alveolar Epithelial Cell Fate (AT2 scRNA-seq)

ABSTRACT: The objective of this study was to compare uncultured primary human alveolar epithelial type 2 cells (AT2s) isolated from lungs to AT2s that were expanded in large-scale.

ORGANISM(S): Homo sapiens

PROVIDER: GSE306194 | GEO | 2025/12/18

REPOSITORIES: GEO

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Aberrant Transitional Alveolar Epithelial Cells Promote Pathogenic Activation of Lung Fibroblasts in Preclinical Fibrosis Modeling (scRNAseq)

Project description:CD44+ and CD44- negative Alveolar type 2 cells (AT2) represent distinct populations in lung fibrosis. To charecterize these cells, we isolated CD44+/- AT2s from WT mice and from fibrotic Sftpc muant lungs and performd RNA sequencing no these populations

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Aberrant Transitional Alveolar Epithelial Cells Promote Pathogenic Activation of Lung Fibroblasts in Preclinical Fibrosis Modeling (Bulk RNA-Seq)

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XCI and sex-biased expression in AT2 cells

Project description:Significant sex differences exist for many lung pathologies, including SARS-CoV-2 related disease (COVID-19) and pulmonary fibrosis, but the mechanistic basis for this remains unclear. Notably, Ace2, the gene encoding angiotensin-converting enzyme 2, an enzyme that plays multiple roles in SARS-CoV-2 pathogenesis, including acting as the major viral receptor, is localized on the X-chromosome. Moreover, prior work in fibroblasts suggested that Ace2 may escape X-Chromosome Inactivation (XCI), which normalizes X-lined gene expression between sexes. Alveolar type 2 cells (AT2s), which play a key role in alveolar lung regeneration, express Ace2, suggesting that aberrant XCI in AT2s could potentially impact sex-biased lung pathology. To that end, we performed RNA-seq on AT2 cells isolated from 4 male and 4 female F1 mus/cast mice. Utilizing allele-specific transcriptomics, we demonstrate that about 50% of expressed X-linked genes in mouse AT2s, including Ace2, escape XCI, the highest levels reported to date. Moreover, we observe dramatic genome-wide expression differences between male and female AT2s, likely influencing both lung physiology and pathophysiologic responses. Taken together, these studies support a renewed focus on AT2s as potential contributor to sex-biased differences in lung disease.

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Advancing Lung Tissue Engineering Through the Discovery of Factors that Control Alveolar Epithelial Cell Fate (AT2 scRNA-seq)

Project description:Advancing Lung Tissue Engineering Through the Discovery of Factors that Control Alveolar Epithelial Cell Fate (AT2 scRNA-seq)

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Transcriptomic analysis of control lung alveolar type 2 cells and constitutively active-BMPR1a overexpressing alveolar type 2 cells

Project description:The Bone Morphogenetic Protein (BMP) signaling pathway functions in lung development and the regeneration of adult tracheal epithelium from basal stem cells. Here, we explore its role in the alveolar region, where Type 2 epithelial cells (AT2s) and Pdgfrα+ Type 2 - associated stromal cells (TASCs) are components of the stem cell niche. We utilize both organoid assays and in vivo alveolar regrowth after pneumonectomy (PNX) - a process requiring proliferation of AT2s and differentiation into Type 1 cells (AT1). BMP signaling is normally active in AT2s and TASCs, transiently declines post-PNX, and is restored during differentiation of AT2s to AT1s. In organoids, BMP4 inhibits AT2 proliferation, while antagonists promote AT2 self-renewal at the expense of differentiation. Gain and loss-of function genetic manipulation reveals that loss of BMP signaling in AT2s after PNX allows their self-renewal but significantly reduces differentiation into AT1s; conversely, increased BMP signaling promotes AT1 formation. The transcriptome analysis of control AT2s and AT2s overexpressing constitutively active-Bmpr1a reveals that 119 genes are upregulated more than two-fold following enhancing BMP signaling. Of these genes, 10 % are normally preferentially expressed in AT1 cells. Of the 25 genes downregulated more than two-fold, 28 % are preferentially expressed in AT2s.

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Project description:Alveolar AT1 and AT2 cells are vital for gas exchange in the lung and become compromised in several common and deadly diseases. While the signals driving differentiation of either cell type have been identified, it remains unclear when and how fate plasticity is regulated in the emerging and adult alveolar epithelium. Here we show AT2s first emerge as singletons at zones between the proximal stalks and distal tips of the embryonic lung that quickly extrude and can traverse the interstitium to connect with nearby epithelium, a process we term interlumenal junctioning. Throughout the late embryonic and early perinatal period, we find that a window of AT2 fate plasticity exists that is closed by the bZIP transcription factor C/EBPα, mediated by its transcriptional suppression of the Notch signaling regulator DLK1. C/EBPα acts on Dlk1 at a novel regulatory site. Further, both Dlk1 and Cebpa are regulated by the polycomb repressive complex (PRC2), and together constitute a novel incoherent feedforward loop that generates a Dlk1 pulse upon downregulation of PRC2. We propose these form a “pulse generator” circuit capable of generating a timed activation of Notch signaling, resulting in a “salt and pepper” pattern of AT1 and AT2 fate. Following injury in the adult lung, we found that C/EBPα downregulation is required for re-accessing AT2 fate plasticity and is mediated by the dominant negative C/EBP family member CHOP. Finally, we observe Cebpa loss also activates a “defender” AT2 state enriched in interferon-stimulated antipathogenic gene expression that is distinct from its reparative state and propose AT2s toggle between these states following infection to robustly protect and repair alveoli.

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Advancing Lung Tissue Engineering Through the Discovery of Factors that Control Alveolar Epithelial Cell Fate (snRNA-seq from recellularized scaffolds)

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Project description:The lung's gas exchange surface is comprised of alveolar AT1 and AT2 cells that are corrupted in several common and deadly diseases. They arise from a bipotent progenitor whose differentiation is thought to be dictated by differential mechanical forces. Here we show the critical determinant is FGF signaling. Fgfr2 is expressed in the developing progenitors in mouse then restricts to nascent AT2 cells and remains on throughout life. Its ligands are expressed in surrounding mesenchyme and can, in the absence of exogenous mechanical cues, induce progenitors to form alveolospheres with intermingled AT2 and AT1 cells. FGF signaling directly and cell autonomously specifies AT2 fate; progenitors lacking Fgfr2 in vitro and in vivo exclusively acquire AT1 fate. Fgfr2 loss in AT2 cells perinatally results in reprogramming to AT1 identity, whereas loss or inhibition later in life triggers AT2 apoptosis and compensatory regeneration. We propose that Fgfr2 signaling selects AT2 fate during development, induces a cell non-autonomous AT1 differentiation signal, then continuously maintains AT2 identity and survival throughout life.

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Project description:We performed bulk transcriptomic profiling of pluripotent stem cell-derived alveolar type 2 cells (iAT2s) and HTII-280-sorted human AT2s cultured with CK+DCI media. We used previously described distal lung directed differentiation protocol to generate alveolar type 2 cells (iAT2s). We used the SPC2-ST-B2 (“SPC2”) line containing a SFTPC-tdTomato knock in reporter. iAT2s were cultured in 3D spheres and at air-liquid interface. Human AT2s were HTII-280-sorted from a pediatric donor lung (13 months old) and an adult, nonsmoker human lung (32 years old) and cultured as spheres in the presence of MRC5s. After deconvolution, we find that iAT2s cultured in ALI correlate more closely to primary cultured AT2s than do iAT2s cultured in 3D spheres on the basis of lung epithelial gene expression.

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