ArticleAmerican journal of physiology. Lung cellular and molecular physiology2012
Interfacial stress affects rat alveolar type II cell signaling and gene expression.
Article in American journal of physiology. Lung cellular and molecular physiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 22 citations in OpenAlex.
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- Acinar micromechanics in health and lung injury: what we have learned from quantitative morphology.Frontiers in physiology · 2023Review
- A multiplex inhalation platform to modelFrontiers in pharmacology · 2023Article
- A New Immortalized Human Alveolar Epithelial Cell Model to Study Lung Injury and Toxicity on a Breathing Lung-On-Chip System.Frontiers in toxicology · 2022Article
- Review
- Human-Based AdvancedFrontiers in medicine · 2021Review
- Lipid-Protein and Protein-Protein Interactions in the Pulmonary Surfactant System and Their Role in Lung Homeostasis.International journal of molecular sciences · 2020Review
- Bioengineering the Blood-gas Barrier.Comprehensive Physiology · 2020Review
- Surfactant Protein B Deficiency Induced High Surface Tension: Relationship between Alveolar Micromechanics, Alveolar Fluid Properties and Alveolar Epithelial Cell Injury.International journal of molecular sciences · 2019Article
- The micromechanics of lung alveoli: structure and function of surfactant and tissue components.Histochemistry and cell biology · 2018Review
- Medium throughput breathing human primary cell alveolus-on-chip model.Scientific reports · 2018Article
- Lung ventilation injures areas with discrete alveolar flooding, in a surface tension-dependent fashion.Journal of applied physiology (Bethesda, Md. : 1985) · 2014Article
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3 authors at 1 institution in 1 country.
Funding
Abstract
Previous work from our group (Ravasio A, Hobi N, Bertocchi C, Jesacher A, Dietl P, Haller T. Am J Physiol Cell Physiol 300: C1456-C1465, 2011.) showed that contact of alveolar epithelial type II cells with an air-liquid interface (I(AL)) leads to a paradoxical situation. It is a potential threat that can cause cell injury, but also a Ca(2+)-dependent stimulus for surfactant secretion. Both events can be explained by the impact of interfacial tensile forces on cellular structures. Here, the strength of this mechanical stimulus became also apparent in microarray studies by a rapid and significant change on the transcriptional level. Cells challenged with an I(AL) in two different ways showed activation/inactivation of cellular pathways involved in stress response and defense, and a detailed Pubmatrix search identified genes associated with several lung diseases and injuries. Altogether, they suggest a close relationship of interfacial stress sensation with current models in alveolar micromechanics. Further similarities between I(AL) and cell stretch were found with respect to the underlying signaling events. The source of Ca(2+) was extracellular, and the transmembrane Ca(2+) entry pathway suggests the involvement of a mechanosensitive channel. We conclude that alveolar type II cells, due to their location and morphology, are specific sensors of the I(AL), but largely protected from interfacial stress by surfactant release.
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