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emphysema

Organoid-Based Expansion of Patient-Derived Primary Alveolar Type-2 Cells for Establishment of Alveolus Epithelial Lung-Chip Cultures

[American Journal of Physiology-Lung Cellular and Molecular Physiology] Investigators isolated primary alveolar type-2 cells (AEC2) from patient-derived lung tissues including those from patients with severe emphysema, using magnetic bead-based selection of cells expressing the AEC2 marker HTII-280.

ISM1 Protects Lung Homeostasis via Cell-Surface GRP78-Mediated Alveolar Macrophage Apoptosis

[Proceedings of the National Academy of Sciences of the United States of America] Researchers reported that absence of isthmin 1 (ISM1) in mice led to increase in both alveolar macrophages number and functional heterogeneity, with enduring lung inflammation, progressive emphysema, and significant lung function decline, phenotypes similar to human obstructive pulmonary disease.

Impact of Reactive Iron in Coal Mine Dust on Oxidant Generation and Epithelial Lung Cell Viability

[Science of the Total Environment] Scientists revealed that reduced iron minerals were widely distributed within samples obtained from Australian coal mines with pyrite and siderite being particularly abundant. Compared with carbon and crystalline silica, the presence of these specific iron minerals were negatively correlated to the viability of both alveolar macrophages and human lung epithelial cells.

Air Pollution-Regulated E-Cadherin Mediates Contact Inhibition of Proliferation via the Hippo Signaling Pathways in Emphysema

[Chemico-Biological interactions] Researchers investigated the role of components of the Hippo signaling pathway for E-cadherin-mediated contact inhibition of proliferation in the lungs after air pollution exposure.

LL-37 and HMGB1 Induce Alveolar Damage and Reduce Lung Tissue Regeneration via RAGE

[American Journal of Physiology-Lung Cellular and Molecular Physiology] The effects of the RAGE ligands LL-37 and HMGB1 were examined on airway inflammation and alveolar tissue damage in wild-type and RAGE deficient mice and on lung damage and repair responses using murine precision cut lung slices and organoids.

LL-37 and HMGB1 Induce Alveolar Damage and Reduce Lung Tissue Regeneration via RAGE

[American Journal of Physiology-Lung Cellular and Molecular Physiology] The effects of the receptor for advanced glycation end-products (RAGE) ligands LL-37 and HMGB1 were examined on airway inflammation and alveolar tissue damage in wild-type and RAGE deficient mice and on lung damage and repair responses using murine precision cut lung slices and organoids.

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