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Repair of airway epithelia requires metabolic rewiring towards fatty acid oxidation

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Mus musculus

PROVIDER: GSE209686 | GEO | 2023/01/31

REPOSITORIES: GEO

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Repair of airway epithelia requires metabolic rewiring towards fatty acid oxidation.

Project description:Epithelial tissues provide front-line barriers shielding the organism from invading pathogens and harmful substances. In the airway epithelium, the combined action of multiciliated and secretory cells sustains the mucociliary escalator required for clearance of microbes and particles from the airways. Defects in components of mucociliary clearance or barrier integrity are associated with recurring infections and chronic inflammation. The timely and balanced differentiation of basal cells into mature epithelial cell subsets is therefore tightly controlled. While different growth factors regulating progenitor cell proliferation have been described, little is known about the role of metabolism in these regenerative processes. Here we show that basal cell differentiation correlates with a shift in cellular metabolism from glycolysis to fatty acid oxidation (FAO). We demonstrate both in vitro and in vivo that pharmacological and genetic impairment of FAO blocks the development of fully differentiated airway epithelial cells, compromising the repair of airway epithelia. Mechanistically, FAO links to the hexosamine biosynthesis pathway to support protein glycosylation in airway epithelial cells. Our findings unveil the metabolic network underpinning the differentiation of airway epithelia and identify novel targets for intervention to promote lung repair.

| S-EPMC9925445 | biostudies-literature

Repair of airway epithelia requires metabolic rewiring towards fatty acid oxidation

Project description:Repair of airway epithelia requires metabolic rewiring towards fatty acid oxidation

2023-01-31 | GSE218663 | GEO

Repair of airway epithelia requires metabolic rewiring towards fatty acid oxidation [I]

Project description:Comparative gene expression profiling analysis of RNA-seq data from CD49f+NGFR+, CD49f-NGFR- cell sorted from differentiated MTEC cultures collected at ALI day 10, and MTEC culture taken at ALI t0

2023-01-31 | GSE209678 | GEO

Repair of airway epithelia requires metabolic rewiring towards fatty acid oxidation [II]

Project description:To test the role of FAO in epithelium differentiation, we assessed genome-wide transcriptional changes in Cpt1a+/- and Cpt1a-/- primary mouse tracheal epithelial cell (mTEC) cultures analysed at the end of the expansion phase (ALI day 0) or at day 5 and 7 post air-exposure by RNA-seq.

2023-01-31 | GSE209684 | GEO

Repair of airway epithelia requires metabolic rewiring towards fatty acid oxidation

Project description:Repair of airway epithelia requires metabolic rewiring towards fatty acid oxidation

| PRJNA862097 | ENA

Repair of airway epithelia requires metabolic rewiring towards fatty acid oxidation

Project description:Repair of airway epithelia requires metabolic rewiring towards fatty acid oxidation

| PRJNA904774 | ENA

Repair of airway epithelia requires metabolic rewiring towards fatty acid oxidation [II]

Project description:Repair of airway epithelia requires metabolic rewiring towards fatty acid oxidation [II]

| PRJNA862106 | ENA

Repair of airway epithelia requires metabolic rewiring towards fatty acid oxidation [I]

Project description:Repair of airway epithelia requires metabolic rewiring towards fatty acid oxidation [I]

| PRJNA862107 | ENA

Representative measles virus infection requires appropriate airway epithelia culture conditions.

Project description:ImportanceFor many years, measles virus (MeV) was assumed to first enter the host via the apical surface of airway epithelial cells and subsequently spread systemically. We and others reported that MeV has an overwhelming preference for entry at the basolateral surface of airway epithelial cells, which led to a fundamental new understanding of how MeV enters a human host. This unexpected observation using well-differentiated primary cultures of airway epithelia from human donors contradicted previous studies using immortalized cultured cells. Here, we show that appropriate differentiation and cell morphology of primary human airway epithelial cells are critical to recapitulate MeV infection patterns and pathogenesis of the in vivo airways. By simply culturing primary cells in media containing serum or passaging primary cultures, erroneous results quickly emerge. These results have broad implications for data interpretation related to respiratory virus infection, spread, and release from human airway epithelial cells.

| S-EPMC10617594 | biostudies-literature

Regulation of lung progenitor plasticity and repair by fatty acid oxidation

Project description:Idiopathic pulmonary fibrosis (IPF) is an age-related interstitial lung disease, characterized by inadequate alveolar regeneration and ectopic bronchiolization. While some molecular pathways regulating lung progenitor cells have been described, the role of metabolic pathways in alveolar regeneration is poorly understood. We report that expression of fatty acid oxidation (FAO) genes significantly diminishes in alveolar epithelial cells of IPF lungs by single-cell RNA sequencing and tissue staining. Genetic and pharmacological inhibition in AT2 cells of carnitine palmitoyltransferase 1a (CPT1a), the rate-limiting enzyme of FAO, promoted mitochondrial dysfunction and acquisition of aberrant intermediate states expressing basaloid, and airway secretory cell markers SCGB1A1, and SCGB3A2. Further, mice with deficiency of CPT1a in AT2 cells show enhanced susceptibility to developing lung fibrosis with an accumulation of epithelial cells expressing markers of intermediate cells, airway secretory cells, and senescence. We found that deficiency of CPT1a causes a decrease in SMAD7 protein levels and TGF-β signaling pathway activation. These findings suggest that the mitochondrial FAO metabolic pathway contributes to the regulation of lung progenitor cell repair responses and deficiency of FAO contributes to aberrant lung repair and the development of lung fibrosis.

2025-02-25 | GSE283885 | GEO

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