scholarly journals Selective targeting of alveolar type II respiratory epithelial cells by anti-surfactant protein-C antibody-conjugated lipoplexes

2015 ◽  
Vol 203 ◽  
pp. 140-149 ◽  
Author(s):  
Yun Wu ◽  
Junyu Ma ◽  
Parker S. Woods ◽  
Nicholas M. Chesarino ◽  
Chang Liu ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Protein C ◽  
Surfactant Protein ◽  
Alveolar Type ◽  
Type Ii ◽  
Respiratory Epithelial Cells ◽  
Surfactant Protein C ◽  
Selective Targeting ◽  
Respiratory Epithelial

Autophagy regulates hyperoxia-induced intracellular accumulation of surfactant protein C in alveolar type II cells

2015 ◽  
Vol 408 (1-2) ◽  
pp. 181-189 ◽  
Author(s):  
Liang Zhang ◽  
Shuang Zhao ◽  
Li-Jie Yuan ◽  
Hong-Min Wu ◽  
Hong Jiang ◽  
...  
Keyword(s):  
Protein C ◽  
Surfactant Protein ◽  
Alveolar Type ◽  
Type Ii Cells ◽  
Type Ii ◽  
Intracellular Accumulation ◽  
Alveolar Type Ii Cells ◽  
Surfactant Protein C

Laminin α-chain expression and basement membrane formation by MLE-15 respiratory epithelial cells

2002 ◽  
Vol 282 (5) ◽  
pp. L1004-L1011 ◽  
Author(s):  
Nguyet M. Nguyen ◽  
Yushi Bai ◽  
Katsumi Mochitate ◽  
Robert M. Senior
Keyword(s):  
Epithelial Cells ◽  
Basement Membrane ◽  
Critical Role ◽  
Basement Membranes ◽  
Alveolar Type ◽  
Type Ii Cells ◽  
Type Ii ◽  
Respiratory Epithelial Cells ◽  
Alveolar Type Ii Cells ◽  
Respiratory Epithelial

Basement membranes have a critical role in alveolar structure and function. Alveolar type II cells make basement membrane constituents, including laminin, but relatively little is known about the production of basement membrane proteins by murine alveolar type II cells and a convenient system is not available to study basement membrane production by murine alveolar type II cells. To facilitate study of basement membrane production, with particular focus on laminin chains, we examined transformed murine distal respiratory epithelial cells (MLE-15), which have many structural and biochemical features of alveolar type II cells. We found that MLE-15 cells produce laminin-α5, a trace amount of laminin-α3, laminins-β1 and -γ1, type IV collagen, and perlecan. Transforming growth factor-β1 significantly induces expression of laminin-α1. When grown on a fibroblast-embedded collagen gel, MLE-15 cells assemble a basement membrane-like layer containing laminin-α5. These findings indicate that MLE-15 cells will be useful in modeling basement membrane production and assembly by alveolar type II cells.

Inhibition of alveolarization and altered pulmonary mechanics in mice expressing GATA-6

2003 ◽  
Vol 285 (6) ◽  
pp. L1246-L1254 ◽  
Author(s):  
Cong Liu ◽  
Machiko Ikegami ◽  
Mildred T. Stahlman ◽  
Chitta R. Dey ◽  
Jeffrey A. Whitsett
Keyword(s):  
Epithelial Cells ◽  
Surfactant Protein ◽  
Mouse Lung ◽  
Pulmonary Mechanics ◽  
Respiratory Epithelial Cells ◽  
Surfactant Protein C ◽  
Spatial Regulation ◽  
Respiratory Epithelial ◽  
Tissue Elastance

GATA-6, a member of a family of zinc finger transcription factors, is expressed in epithelial cells of the developing lung. To further assess the role of GATA-6 in lung morphogenesis, GATA-6 was expressed in respiratory epithelial cells of the developing mouse lung under control of the surfactant protein C promoter (hSP-CGATA-6 mice). Although GATA-6 did not alter lung morphology at embryonic day 18.5, defects in alveolar septation were observed early in the neonatal period, and air space enlargement persisted to adulthood. Airway resistance, airway elastance, tissue damping, and tissue elastance were significantly decreased, and lung volumes were significantly increased at 12 wk of age. Normal postnatal morphogenesis of the lung depends upon precise temporal-spatial regulation of GATA-6.

β-Catenin regulates differentiation of respiratory epithelial cells in vivo

2005 ◽  
Vol 289 (6) ◽  
pp. L971-L979 ◽  
Author(s):  
Michael L. Mucenski ◽  
Jennifer M. Nation ◽  
Angela R. Thitoff ◽  
Valérie Besnard ◽  
Yan Xu ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Goblet Cell ◽  
Alveolar Type ◽  
Type Ii ◽  
Respiratory Epithelial Cells ◽  
Cell Hyperplasia ◽  
Goblet Cell Hyperplasia ◽  
Air Space ◽  
Respiratory Epithelial ◽  
Conducting Airways

An activated form of β-catenin [CatnbΔ(ex3)] was expressed in respiratory epithelial cells of the developing lung. Although morphogenesis was not altered at birth, air space enlargement and epithelial cell dysplasia were observed in the early postnatal period and persisted into adulthood. The CatnbΔ(ex3) protein caused squamous, cuboidal, and goblet cell dysplasia in intrapulmonary conducting airways. Atypical epithelial cells that stained for surfactant pro protein C (pro-SP-C) and had morphological characteristics of alveolar type II cells were observed in bronchioles of the transgenic mice. CatnbΔ(ex3) inhibited expression of Foxa2 and caused goblet cell hyperplasia associated with increased staining for mucins and the MUC5A/C protein. In vitro, both wild type and activated β-catenin negatively regulated the expression of the Foxa2 promoter. CatnbΔ(ex3) also caused pulmonary tumors in adult mice. Activation of β-catenin caused ectopic differentiation of alveolar type II-like cells in conducting airways, goblet cell hyperplasia, and air space enlargement, demonstrating a critical role for the Wnt/β-catenin signal transduction pathway in the differentiation of the respiratory epithelium in the postnatal lung.

Synthesis and processing of hydrophobic surfactant protein C by isolated rat type II cells

1995 ◽  
Vol 269 (6) ◽  
pp. L744-L753 ◽  
Author(s):  
M. F. Beers ◽  
C. Lomax
Keyword(s):  
Protein C ◽  
Brefeldin A ◽  
Surfactant Protein ◽  
Alveolar Type ◽  
Type Ii Cells ◽  
Metabolic Labeling ◽  
Type Ii ◽  
Surfactant Protein C ◽  
Adult Rat ◽  
The Media

Surfactant protein C (SP-C) is a 3.7-kDa hydrophobic peptide isolated from organic extracts of pulmonary surfactant which is secreted by alveolar type II cells after synthesis and posttranslational processing of a 21-kDa proSP-C peptide (SP-C21). Previously characterized epitope-specific proSP-C antisera were used to study early proteolytic steps of proSP-C processing by adult rat type II cells. Western blotting and immunocytochemistry using anti-NPROSP-C (epitope = Met10-Glu23) each demonstrated marked attenuation of proSP-C protein expression by culture on plastic. Processing was therefore studied by metabolic labeling of freshly isolated type II cells maintained in suspension in serum-free media. With the use of anti-NPROSP-C, immunoprecipitation of cell lysates continuously labeled for 4 h with [35S]methionine demonstrated radiolabeled bands of M(r) 21, 16, and 10-6,000 while anti-CTERMSP-C (epitope = Ser149-Ser166) failed to detect 35S-bands of M(r) < 16,000. Pulse-chase studies demonstrated synthesis of 35S-proSP-C21 with a time-dependent dependent appearance of 16-kDa and 10- to 6-kDa forms which was blocked by addition of brefeldin A. SP-C precursors were not detected in the media. Quantitative analysis of the major bands by direct beta-counting indicated a precursor-product relationship between SP-C21 and SP-C16. These results demonstrate the utility of freshly isolated type II cells for characterization of SP-C synthetic pathways and show that early proSP-C processing events include synthesis of a 21-kDa primary translation product followed by extensive intracellular proteolysis of the proSP-C COOH-terminal in subcellular compartments of type II cells which are distal to the trans-Golgi network.

Surfactant Protein C Is Expressed in Alveolar Type II Cells but Not in Clara Cells of Rat Lung

1992 ◽  
Vol 6 (6) ◽  
pp. 594-600 ◽  
Author(s):  
Moshe Kalina ◽  
Robert J. Mason ◽  
John M. Shannon
Keyword(s):  
Protein C ◽  
Surfactant Protein ◽  
Alveolar Type ◽  
Type Ii Cells ◽  
Type Ii ◽  
Clara Cells ◽  
Rat Lung ◽  
Alveolar Type Ii Cells ◽  
Surfactant Protein C

Association of surfactant protein C with isolated alveolar type II cells

1995 ◽  
Vol 1255 (1) ◽  
pp. 16-22 ◽  
Author(s):  
Ricardo A. Pinto ◽  
Samuel Hawgood ◽  
John A. Clements ◽  
Bradley J. Benson ◽  
Asha Naidu ◽  
...  
Keyword(s):  
Protein C ◽  
Surfactant Protein ◽  
Alveolar Type ◽  
Type Ii Cells ◽  
Type Ii ◽  
Alveolar Type Ii Cells ◽  
Surfactant Protein C

scholarly journals Transitional human alveolar type II epithelial cells suppress extracellular matrix and growth factor gene expression in lung fibroblasts

2019 ◽  
Vol 317 (2) ◽  
pp. L283-L294 ◽  
Author(s):  
Kelly A. Correll ◽  
Karen E. Edeen ◽  
Rachel L. Zemans ◽  
Elizabeth F. Redente ◽  
Karina A. Serban ◽  
...  
Keyword(s):  
Growth Factor ◽  
Epithelial Cells ◽  
Surfactant Protein ◽  
Lung Fibroblasts ◽  
Alveolar Type ◽  
Type I ◽  
Type Ii Cells ◽  
Type Ii ◽  
Alveolar Type Ii Cells ◽  
I Cells

Epithelial-fibroblast interactions are thought to be very important in the adult lung in response to injury, but the specifics of these interactions are not well defined. We developed coculture systems to define the interactions of adult human alveolar epithelial cells with lung fibroblasts. Alveolar type II cells cultured on floating collagen gels reduced the expression of type 1 collagen (COL1A1) and α-smooth muscle actin (ACTA2) in fibroblasts. They also reduced fibroblast expression of hepatocyte growth factor (HGF), fibroblast growth factor 7 (FGF7, KGF), and FGF10. When type II cells were cultured at an air-liquid interface to maintain high levels of surfactant protein expression, this inhibitory activity was lost. When type II cells were cultured on collagen-coated tissue culture wells to reduce surfactant protein expression further and increase the expression of some type I cell markers, the epithelial cells suppressed transforming growth factor-β (TGF-β)-stimulated ACTA2 and connective tissue growth factor (CTGF) expression in lung fibroblasts. Our results suggest that transitional alveolar type II cells and likely type I cells but not fully differentiated type II cells inhibit matrix and growth factor expression in fibroblasts. These cells express markers of both type II cells and type I cells. This is probably a normal homeostatic mechanism to inhibit the fibrotic response in the resolution phase of wound healing. Defining how transitional type II cells convert activated fibroblasts into a quiescent state and inhibit the effects of TGF-β may provide another approach to limiting the development of fibrosis after alveolar injury.

Histone deacetylase inhibitor restores surfactant protein-C expression in alveolar-epithelial type II cells and attenuates bleomycin-induced pulmonary fibrosisin vivo

2015 ◽  
Vol 41 (8) ◽  
pp. 422-434 ◽  
Author(s):  
Chiharu Ota ◽  
Mitsuhiro Yamada ◽  
Naoya Fujino ◽  
Hozumi Motohashi ◽  
Yukiko Tando ◽  
...  
Keyword(s):  
Histone Deacetylase ◽  
Histone Deacetylase Inhibitor ◽  
Protein C ◽  
Surfactant Protein ◽  
Type Ii Cells ◽  
Type Ii ◽  
Surfactant Protein C ◽  
Alveolar Epithelial ◽  
Deacetylase Inhibitor
Sign in / Sign up

Export Citation Format

Share Document