Keratinocyte growth factor modulates alveolar epithelial cell phenotype in vitro: expression of aquaporin 5.

@article{Borok1998KeratinocyteGF,
  title={Keratinocyte growth factor modulates alveolar epithelial cell phenotype in vitro: expression of aquaporin 5.},
  author={Zea Borok and Richard L. Lubman and Spencer I. Danto and X. L. Zhang and Stephanie M. Zabski and Landon Stuart King and D. M. Lee and Peter Agre and Edward D. Crandall},
  journal={American journal of respiratory cell and molecular biology},
  year={1998},
  volume={18 4},
  pages={
          554-61
        }
}
We investigated the role of keratinocyte growth factor (KGF) in regulation of alveolar epithelial cell (AEC) phenotype in vitro. Effects of KGF on cell morphology, expression of surfactant apoproteins A, B, and C (SP-A, -B, and -C), and expression of aquaporin 5 (AQP5), a water channel present in situ on the apical surface of alveolar type I (AT1) cells but not expressed in alveolar type II (AT2) cells, were evaluated in AECs grown in primary culture. Observations were made on AEC monolayers… 

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Modulation of T1α expression with alveolar epithelial cell phenotype in vitro.

It is demonstrated that both soluble factors and alterations in cell shape modulate T1α expression in parallel with AEC phenotype and provide further support for the concept that transdifferentiation between AT2 and AT1 cell phenotypes is at least partially reversible.

Keratinocyte growth factor enhances barrier function without altering claudin expression in primary alveolar epithelial cells.

A novel mechanism by which KGF enhances alveolar barrier function, modulation of the actin cytoskeleton is supported.

Effects of KGF on alveolar epithelial cell transdifferentiation are mediated by JNK signaling.

Results indicate that retention of the AT2 cell phenotype by KGF involves c-Jun and suggest that activation of c- Jun kinase may be an important determinant of maintenance of AT1 cell phenotype.

Modulation of pulmonary alveolar type II cell phenotype and communication by extracellular matrix and KGF.

The parallel changes in intercellular Ca(2+) signaling with cell differentiation suggest that cell signaling mechanisms are an intrinsic component of lung alveolar cell phenotype and may be vital to the lung recovery and repair process in vivo.

Surfactant homeostasis is maintained in vivo during keratinocyte growth factor-induced rat lung type II cell hyperplasia.

It is concluded that under rHuKGF-induced AEII proliferation intracellular surfactant was decreased per single cell, whereas a constant amount was maintained per unit lung volume, suggesting that surfactants homeostasis is regulated at the level of phospholipid transport processes, for example, secretion and reuptake.

Characterization of mouse alveolar epithelial cell monolayers.

It is demonstrated that AT1 cell-like MAECM grown on laminin 5-coated polycarbonate filters exhibit active and passive transport properties that likely reflect the properties of intact mouse alveolar epithelium.

EXTRACELLULAR MATRIX-DRIVEN ALVEOLAR EPITHELIAL CELL DIFFERENTIATION IN VITRO

It is concluded that in vitro, AT2 cells exhibited phenotypic plasticity that included an intermediate cell type with both AT1 and AT2 cell characteristics independent of day 7 phenotype; both collagen and Ln5 were needed to promote the development of an AT2-like phenotype at day 7; and components of the extracellular matrix (ECM) contribute to Phenotypic switching of alveolar cells in culture.

Expression and biological activity of ABCA1 in alveolar epithelial cells.

P pneumocytes with markers for the type I phenotype contained functional ABCA1 protein, released lipid to apoA-I protein, and were capable of producing particles resembling nascent high-density lipoprotein, indicating an important role for ABCA 1 in the maintenance of lung lipid homeostasis.

Differentiation of human alveolar epithelial cells in primary culture: morphological characterization and synthesis of caveolin-1 and surfactant protein-C

It is suggested that the culture may serve as a suitable model to study epithelial transport or cell biological processes in human alveolar cells to characterize a primary cell culture for in vitro model studying pulmonary drug delivery.

Phenotypic control of gap junctional communication by cultured alveolar epithelial cells.

Type II cells dynamically alter gap junctional communication, and distinct alveolar epithelial cell phenotypes express different connexins.
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