ArticleDisease models & mechanisms2015
Enolase 1 (ENO1) and protein disulfide-isomerase associated 3 (PDIA3) regulate Wnt/β-catenin-driven trans-differentiation of murine alveolar epithelial cells.
Article in Disease models & mechanisms, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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Who cites it
36 citing papers in PubMed, 59 citations in OpenAlex.
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- PGE2 Produced by Exogenous MSCs Promotes Immunoregulation in ARDS Induced by Highly Pathogenic Influenza A through Activation of the Wnt-β-Catenin Signaling Pathway.International journal of molecular sciences · 2023Review
- Pulmonary endogenous progenitor stem cell subpopulation: Physiology, pathogenesis, and progress.Journal of intensive medicine · 2023Review
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- The arginine methyltransferase PRMT7 promotes extravasation of monocytes resulting in tissue injury in COPD.Nature communications · 2022Article
- NR4A1 Promotes LPS-Induced Acute Lung Injury through Inhibition of Opa1-Mediated Mitochondrial Fusion and Activation of PGAM5-Related Necroptosis.Oxidative medicine and cellular longevity · 2022Article
- A drug screen with approved compounds identifies amlexanox as a novel Wnt/β-catenin activator inducing lung epithelial organoid formation.British journal of pharmacology · 2021Article
- Enolase 1, a Moonlighting Protein, as a Potential Target for Cancer Treatment.International journal of biological sciences · 2021Review
- Depletion ofFrontiers in cell and developmental biology · 2021Article
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- TRPV4 channels are essential for alveolar epithelial barrier function as protection from lung edema.JCI insight · 2020Article
- Decreased secretion and profibrotic activity of tubular exosomes in diabetic kidney disease.American journal of physiology. Renal physiology · 2020Article
- Alveolar regeneration through a Krt8+ transitional stem cell state that persists in human lung fibrosis.Nature communications · 2020Article
- Genome-wide integration of microRNA and transcriptomic profiles of differentiating human alveolar epithelial cells.American journal of physiology. Lung cellular and molecular physiology · 2020Article
- Chronic WNT/β-catenin signaling induces cellular senescence in lung epithelial cells.Cellular signalling · 2020Article
- Endoplasmic reticulum stress and glutathione therapeutics in chronic lung diseases.Redox biology · 2020Review
- Alveolar Epithelial Type II Cells as Drivers of Lung Fibrosis in Idiopathic Pulmonary Fibrosis.International journal of molecular sciences · 2020Review
- Pathological consequences of the unfolded protein response and downstream protein disulphide isomerases in pulmonary viral infection and disease.Journal of biochemistry · 2020Review
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Authors and funding
5 authors at 4 institutions in 2 countries.
Funding
Abstract
The alveolar epithelium represents a major site of tissue destruction during lung injury. It consists of alveolar epithelial type I (ATI) and type II (ATII) cells. ATII cells are capable of self-renewal and exert progenitor function for ATI cells upon alveolar epithelial injury. Cell differentiation pathways enabling this plasticity and allowing for proper repair, however, are poorly understood. Here, we applied proteomics, expression analysis and functional studies in primary murine ATII cells to identify proteins and molecular mechanisms involved in alveolar epithelial plasticity. Mass spectrometry of cultured ATII cells revealed a reduction of carbonyl reductase 2 (CBR2) and an increase in enolase 1 (ENO1) and protein disulfide-isomerase associated 3 (PDIA3) protein expression during ATII-to-ATI cell trans-differentiation. This was accompanied by increased Wnt/β-catenin signaling, as analyzed by qRT-PCR and immunoblotting. Notably, ENO1 and PDIA3, along with T1α (podoplanin; an ATI cell marker), exhibited decreased protein expression upon pharmacological and molecular Wnt/β-catenin inhibition in cultured ATII cells, whereas CBR2 levels were stabilized. Moreover, we analyzed primary ATII cells from mice with bleomycin-induced lung injury, a model exhibiting activated Wnt/β-catenin signaling in vivo. We observed reduced CBR2 significantly correlating with surfactant protein C (SFTPC), whereas ENO1 and PDIA3 along with T1α were increased in injured ATII cells. Finally, siRNA-mediated knockdown of ENO1, as well as PDIA3, in primary ATII cells led to reduced T1α expression, indicating diminished cell trans-differentiation. Our data thus identified proteins involved in ATII-to-ATI cell trans-differentiation and suggest a Wnt/β-catenin-driven functional role of ENO1 and PDIA3 in alveolar epithelial cell plasticity in lung injury and repair.
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