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Effect of knockdown of junctional genes JUP and PLEC on Small Airway Epithelial Cells (SAECs) in the context of epithelial desquamation in distal bronchioles of Idiopathic Pulmonary fibrosis (IPF) patients

ABSTRACT: Effect of knockdown of junctional genes JUP and PLEC on Small Airway Epithelial Cells (SAECs) in the context of epithelial desquamation in distal bronchioles of Idiopathic Pulmonary fibrosis (IPF) patients

PROVIDER: PRJNA1113677 | ENA |

REPOSITORIES: ENA

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Effect of knockdown of junctional genes JUP and PLEC on Small Airway Epithelial Cells (SAECs) in the context of epithelial desquamation in distal bronchioles of Idiopathic Pulmonary fibrosis (IPF) patients

Project description:JUP and PLEC are downregulated in the distal bronchioles of IPF patients. To understand the relevance of this in the epithelial sloughing (desquamation) phenotype observed in distal bronchioles of IPF patients, we knockeddown JUP and PLEC in small airway epithelial cells thats are isolated from distal bronchioles of human airway epithelium (Lonza). Bulk RNA sequencing of JUP vs Scrambled and PLEC vs Scrambled were performed. The transriptomic data suggests that JUP transcriptionally regulates the matrix synthesis and the transcription of other junctional genes in SAECs. However, no significant effect of PLEC knockdown on transcription of matrix genes, a significant reduction in junctional gene transcripts were observed in PLEC knockdown. These findings suggest that JUP and PLEC may play key roles in the regulation of epithelial integrity during homeostasis, and when desrupted can lead to epithelial desquamation.

2025-09-01 | GSE267943 | GEO

Spatial transcriptomics of the distal lung bronchioles unravel the mechanisms underlying epithelial desquamation in idiopathic pulmonary fibrosis (IPF)

Project description:One histopathological hallmark seen in end-stage IPF within the distal bronchioles is epithelial desquamation, a process in which the epithelial cells detach from their basement membrane. We performed spatial transcriptomics to profile the distal bronchiolar epithelium of the IPF lung and compared it to healthy lung bronchiolar epithelium. Our analysis has revealed crucial pathways leading to epithelial desquamation.

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Spatial transcriptomics of the distal lung bronchioles unravel the mechanisms underlying epithelial desquamation in idiopathic pulmonary fibrosis (IPF)

Project description:Spatial transcriptomics of the distal lung bronchioles unravel the mechanisms underlying epithelial desquamation in idiopathic pulmonary fibrosis (IPF)

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Single cell RNA Sequencing Identifies G-protein Coupled Receptor 87 as a Basal Cell Marker Expressed in Distal Honeycomb Cysts in Idiopathic Pulmonary Fibrosis

Project description:Idiopathic Pulmonary Fibrosis (IPF) is a devastating and life-threatening lung disease characterized by epithelial reprogramming and increased extracellular matrix deposition leading to loss of lung function. A prominent histopathological structure in the IPF lung are aberrant bronchioles filled with mucus, referred to as honeycomb cysts. These heterogeneous bronchiolized areas feature clusters of simple epithelium with Keratin (KRT)5+ basal-like cells interspersed with pseudostratified epithelium containing differentiated, hyperplastic epithelial cells as well as aberrant ciliated cells. Recent single-cell RNA sequencing studies of the lung epithelium shed further light into cellular subtypes unique to IPF, including basaloid KRT5-/KRT17+ cells present in the distal lung. However, IPF distal bronchiole cell subtypes still remain poorly characterized and their disease contribution remains underinvestigated. Using single-cell RNA sequencing of enriched EpCAM+ lung cells of the distal IPF lung, we identified G-protein coupled receptor (GPR) 87, as a marker of distal bronchioles and KRT5+ IPF basal cells contributing to impaired airway differentiation and honeycombing.

2022-05-01 | GSE190889 | GEO

Idiopathic pulmonary fibrosis (IPF)

Project description:Idiopathic pulmonary fibrosis (IPF) is a disease related to AT2 cell. We used flow cytometry to analyze the epithelial component of donor and IPF lungs. From the live cells, we first excluded the CD31PosCD45Pos and then selected the EPCAMPos cells for further analysis using the human AT2 cell marker HTll-280 and the surface marker PD-L1. Our data indicate that, the bona fide differentiated AT2 cells (HTll-280High PD-L1Neg), were drastically reduced in the context of IPF. More interestingly, the number of HTll-280Low/Neg PD-L1High was drastically increased, suggesting that HTll-280Low PD-L1High epithelial cells could represent a pool of progenitors linked to the deficient AT2 lineage. The aim of this experiment is further characterization of AT2 and PDL1+ cells in donor and IPF.

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The profile of miRNAs in lung fibroblast-derived extracellular vesicles from idiopathic pulmonary fibrosis (IPF) patients or non-IPF individuals.

Project description:Accelerated senescence in lung epithelial cells is known to play a key role in the pathogenesis of idiopathic pulmonary fibrosis (IPF). However, the exact mechanisms underlying the IPF-related epithelial cell phenotype have yet to be elucidated. Increasing evidence supports the concept that extracellular vesicles (EVs), including exosomes and microvesicles, mediate intercellular communication that contributes to diverse aspects of physiology and pathogenesis. Here, we demonstrate that lung fibroblasts (LFs) from IPF patients accelerate epithelial cell senescence via EV-mediated transfer of LF-derived pathogenic cargo to lung epithelial cells. Mechanistically, IPF LF-derived EVs increase mitochondrial reactive oxygen species (mtROS) and associated mitochondrial damage in lung epithelial cells, leading to mtROS-mediated activation of the DNA damage response and subsequent epithelial cell senescence. We show that IPF LF-derived EVs contain elevated levels of miR-23b-3p and miR-494-3p that are responsible for suppressing SIRT3, resulting in the EV-induced phenotypic changes of lung epithelial cells. Furthermore, we observe that miR-23b-3p and miR-494-3p expression increases in lung epithelial cells from IPF patients’ lungs. Finally, the levels of miR-23b-3p and 494-3p found in IPF LF-derived EVs correlate positively with IPF disease severity. These findings reveal that the accelerated epithelial cell mitochondrial damage and senescence observed during IPF pathogenesis are caused by a novel mechanism in which SIRT3 is suppressed by miR-containing EVs derived from IPF fibroblasts.

2020-08-04 | GSE124665 | GEO

Idiopathic pulmonary fibrosis (IPF)

Project description:Idiopathic pulmonary fibrosis (IPF)

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Generation of expandable multipotential distal lung progenitors from human pluripotent stem cells that model idiopathic pulmonary fibrosis [scRNA-Seq]

Project description:Human lungs contain unique cell populations in distal respiratory airways and terminal bronchioles (RA/TRB) that accumulate in patients with lung injury and idiopathic pulmonary fibrosis (IPF), a lethal lung disease. As these populations are absent in rodents, deeper understanding requires a human in vitro model. Here we convert human pluripotent stem cells into expandable spheres, called induced respiratory airway progenitors (iRAPs), consisting of ~99% RA/TRB-associated cell types. One hPSC can give rise to 1010 iRAP cells. We differentiate iRAPs through a stage consistent with transitional AT2 like cells into a population corresponding to mature AT1 cells with 95% purity. iRAPs with deletion of HPS1, which causes pulmonary fibrosis in humans, replicate the aberrant differentiation and recruitment of profibrotic fibroblasts observed in IPF, indicating that intrinsic dysfunction of RA/TRB-associated alveolar progenitors contributes to HPS1-related IPF. iRAPs may provide a system suitable for IPF drug discovery and validation.

2025-01-13 | GSE245722 | GEO

Differential Lysotracker Uptake Defines Two Populations of Distal Epithelial Cells in Idiopathic Pulmonary Fibrosis

Project description:For this project alveolar epithelial type-II cells (AT-II) were FACS sorted from 8 donor lungs and 6 fibrotic lungs. The main goals of this experiment is to identify differences in transcriptional programms in AT-II cells from human donor and IPF patients.

2021-10-12 | GSE185691 | GEO

microRNA expression profiles in Idiopathic Pulmonary Fibrosis (IPF)

Project description:Idiopathic pulmonary fibrosis (IPF) is a lethal fibrotic lung disease characterized by enhanced fibroblast proliferation, collagen synthesis, extracellular matrix deposition. We obtained 28 IPF patient lung tissue samples from the Lung Tissue Research Consortium (LTRC). Here we determined the miRNA expression profiles in these IPF lung samples.

2019-04-02 | GSE129126 | GEO

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