ArticleAmerican journal of physiology. Lung cellular and molecular physiology2013
Transdifferentiation of alveolar epithelial type II to type I cells is controlled by opposing TGF-β and BMP signaling.
Article in American journal of physiology. Lung cellular and molecular physiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 69 papers.
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Who cites it
69 citing papers in PubMed, 110 citations in OpenAlex.
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- Role of BMPR2 Mutation in Lung Organoid Differentiation.Biomedicines · 2025Article
- Physiological Modeling of the Vascularized Human Lung Organoid.American journal of respiratory cell and molecular biology · 2025Article
- Therapeutic targeting of TGF-β in lung cancer.The FEBS journal · 2025Review
- Influenza B virus infection alters the regenerative potential of murine alveolar type 2 pneumocytes.mBio · 2025Article
- YAP activity protects against ventilator-induced lung injury.Frontiers in physiology · 2025Article
- Alveolar epithelial type 2 cells in acute lung injury and acute respiratory distress syndrome: spatiotemporal fate and regulation.Burns & trauma · 2025Review
- PCLAF-DREAM drives alveolar cell plasticity for lung regeneration.Nature communications · 2024Article
- Interleukin-11 causes alveolar type 2 cell dysfunction and prevents alveolar regeneration.Nature communications · 2024Article
- Long-term alterations in lung epithelial cells after EL-RSV infection exacerbate allergic responses through IL-1β-induced pathways.Mucosal immunology · 2024Article
- Generation of human alveolar epithelial type I cells from pluripotent stem cells.Cell stem cell · 2024Article
- Breathing new life into the study of COPD with genes identified from genome-wide association studies.European respiratory review : an official journal of the European Respiratory Society · 2024Review
- Screening of factors inducing alveolar type 1 epithelial cells using human pluripotent stem cells.Stem cell reports · 2024Article
9 more citing papers are in PubMed but not listed here.
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Alveolar epithelial type II (ATII) cells are essential for maintaining normal lung homeostasis because they produce surfactant, express innate immune proteins, and can function as progenitors for alveolar epithelial type I (ATI) cells. Although autocrine production of transforming growth factor (TGF)-β1 has been shown to promote the transdifferentiation of primary rat ATII to ATI cells in vitro, mechanisms controlling this process still remain poorly defined. Here, evidence is provided that Tgf-β1, -2, -3 mRNA and phosphorylated SMAD2 and SMAD3 significantly increase as primary cultures of mouse ATII cells transdifferentiate to ATI cells. Concomitantly, bone morphogenetic protein (Bmp)-2 and -4 mRNA, and phosphorylated SMAD1/5/8 expression decrease. Exogenously supplied recombinant human TGF-β1 inhibited BMP signaling and enhanced transdifferentiation by promoting the loss of ATII cell-specific gene expression and weakly stimulating ATI cell-specific gene expression. On the other hand, exogenously supplied recombinant human BMP-4 inhibited TGF-β signaling and delayed transdifferentiation by inhibiting the gain in ATI cell-specific gene expression and weakly delaying the loss of ATII cell-specific gene expression. In mouse lung epithelial (MLE15) cells, small-interfering RNA (siRNA) knockdown of TGF-β receptor type-1 enhanced basal expression of ATII genes while siRNA RNA knockdown of BMP receptors type-1a and -1b enhanced basal expression of ATI genes. Together, these results suggest that the rate of ATII cell transdifferentiation is controlled by the opposing actions of BMP and TGF-β signaling that switch during the process of transdifferentiation.
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