We are analyzing https://link.springer.com/article/10.1186/rr36.

Title:
Alveolar epithelial type II cell: defender of the alveolus revisited | Respiratory Research
Description:
In 1977, Mason and Williams developed the concept of the alveolar epithelial type II (AE2) cell as a defender of the alveolus. It is well known that AE2 cells synthesise, secrete, and recycle all components of the surfactant that regulates alveolar surface tension in mammalian lungs. AE2 cells influence extracellular surfactant transformation by regulating, for example, pH and [Ca2+] of the hypophase. AE2 cells play various roles in alveolar fluid balance, coagulation/fibrinolysis, and host defence. AE2 cells proliferate, differentiate into AE1 cells, and remove apoptotic AE2 cells by phagocytosis, thus contributing to epithelial repair. AE2 cells may act as immunoregulatory cells. AE2 cells interact with resident and mobile cells, either directly by membrane contact or indirectly via cytokines/growth factors and their receptors, thus representing an integrative unit within the alveolus. Although most data support the concept, the controversy about the character of hyperplastic AE2 cells, reported to synthesise profibrotic factors, proscribes drawing a definite conclusion today.
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Keywords {🔍}

google, scholar, cells, alveolar, cell, surfactant, lung, type, epithelial, pulmonary, physiol, rat, respir, protein, biol, growth, expression, lamellar, spa, mol, factor, bodies, human, secretion, surface, proteins, alveolus, injury, proliferation, apoptosis, lungs, review, membrane, vitro, receptor, pneumocytes, regulation, mason, extracellular, processing, epithelium, macrophages, differentiation, exp, res, williams, reported, vivo, edited, invest,

Topics {✒️}

granulocyte-macrophage colony-stimulating factor sp-b-linked microsatellite markers e-cadherin-dependent growth suppression ae2-cell-related pulmonary dysfunction transforming growth factor-beta1 transforming growth factor-beta ae2-cell-derived tgf-β [170] platelet-derived growth factor transforming growth factor-alpha tumour necrosis factor-alpha regulating t-cell activity parathyroid hormone-related protein tumor necrosis factor-alpha cell-type-specific lectins lateral cell–cell contacts epithelial cell-fibroblast interactions lps-induced nitrite production β2-integrins cd11b/cd18 indirect cell–cell interactions amphipathic gamma-glutamyl transferase high-conductance chloride channels albumin-binding immunoglobulin receptor camp-dependent protein kinase epitope-specific antipeptide antibodies individual subfrac-tions represent bleomycin-induced lung injury mercury-sensitive water channels adenovector-mediated gene transfer full size image radiation-induced pulmonary fibrosis differentially regulates ifn-γ de brum-fernandes aj ancient anti-adhesive material specific acid alpha-glucosidase ae2-cell-derived factors rat intra-alveolar surfactant ae2-cell-induced apoptosis fundamental ultrastructure/microautoradiography study ae2-cell-derived insulin alveolar surface-active material ae2 cell double-labelled type ii pneumocytes type-ii pneumocytes growth factor-ii no2-challenged rat lungs tumour necrosis factor amazingly regular phospholipid/sp pneumocyte type ii type ii cells modulate macrophage functions

Schema {🗺️}

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      headline:Alveolar epithelial type II cell: defender of the alveolus revisited
      description:In 1977, Mason and Williams developed the concept of the alveolar epithelial type II (AE2) cell as a defender of the alveolus. It is well known that AE2 cells synthesise, secrete, and recycle all components of the surfactant that regulates alveolar surface tension in mammalian lungs. AE2 cells influence extracellular surfactant transformation by regulating, for example, pH and [Ca2+] of the hypophase. AE2 cells play various roles in alveolar fluid balance, coagulation/fibrinolysis, and host defence. AE2 cells proliferate, differentiate into AE1 cells, and remove apoptotic AE2 cells by phagocytosis, thus contributing to epithelial repair. AE2 cells may act as immunoregulatory cells. AE2 cells interact with resident and mobile cells, either directly by membrane contact or indirectly via cytokines/growth factors and their receptors, thus representing an integrative unit within the alveolus. Although most data support the concept, the controversy about the character of hyperplastic AE2 cells, reported to synthesise profibrotic factors, proscribes drawing a definite conclusion today.
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