Luminal surfaces of fetal rat alveolar type II and clara lung cells react with antibody to heymann nephritis antigen

1991 ◽  
Vol 10 (4) ◽  
pp. 260-266 ◽  
Author(s):  
Robert V. Kotas ◽  
John J. Kanalas ◽  
Fermin O. Tio ◽  
Sudesh P. Makker
Keyword(s):  
Lung Cells ◽  
Alveolar Type ◽  
Type Ii ◽  
Heymann Nephritis ◽  
Fetal Rat

scholarly journals An improved method for the isolation of rat alveolar type II lung cells: Use in the Comet assay to determine DNA damage induced by cigarette smoke

2015 ◽  
Vol 72 (1) ◽  
pp. 141-149 ◽  
Author(s):  
Annette Dalrymple ◽  
Patricia Ordoñez ◽  
David Thorne ◽  
Debbie Dillon ◽  
Clive Meredith
Keyword(s):  
Dna Damage ◽  
Comet Assay ◽  
Cigarette Smoke ◽  
Lung Cells ◽  
Alveolar Type ◽  
Type Ii ◽  
Improved Method

scholarly journals Paracrine Regulation of Alveolar Epithelial Damage and Repair Responses by Human Lung-Resident Mesenchymal Stromal Cells

Cells ◽  
2021 ◽  
Vol 10 (11) ◽  
pp. 2860
Author(s):  
Dennis M. L. W. Kruk ◽  
Marissa Wisman ◽  
Jacobien A. Noordhoek ◽  
Mehmet Nizamoglu ◽  
Marnix R. Jonker ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Mesenchymal Stromal Cells ◽  
Lung Tissue ◽  
Stromal Cells ◽  
Wound Repair ◽  
Lung Cells ◽  
Alveolar Type ◽  
Type Ii ◽  
Epithelial Damage ◽  
Alveolar Epithelial

COPD is characterized by irreversible lung tissue damage. We hypothesized that lung-derived mesenchymal stromal cells (LMSCs) reduce alveolar epithelial damage via paracrine processes, and may thus be suitable for cell-based strategies in COPD. We aimed to assess whether COPD-derived LMSCs display abnormalities. LMSCs were isolated from lung tissue of severe COPD patients and non-COPD controls. Effects of LMSC conditioned-medium (CM) on H2O2-induced, electric field- and scratch-injury were studied in A549 and NCI-H441 epithelial cells. In organoid models, LMSCs were co-cultured with NCI-H441 or primary lung cells. Organoid number, size and expression of alveolar type II markers were assessed. Pre-treatment with LMSC-CM significantly attenuated oxidative stress-induced necrosis and accelerated wound repair in A549. Co-culture with LMSCs supported organoid formation in NCI-H441 and primary epithelial cells, resulting in significantly larger organoids with lower type II-marker positivity in the presence of COPD-derived versus control LMSCs. Similar abnormalities developed in organoids from COPD compared to control-derived lung cells, with significantly larger organoids. Collectively, this indicates that LMSCs’ secretome attenuates alveolar epithelial injury and supports epithelial repair. Additionally, LMSCs promote generation of alveolar organoids, with abnormalities in the supportive effects of COPD-derived LMCS, reflective of impaired regenerative responses of COPD distal lung cells.

Ascorbate uptake by isolated rat alveolar macrophages and type II cells

1983 ◽  
Vol 54 (1) ◽  
pp. 208-214 ◽  
Author(s):  
V. Castranova ◽  
J. R. Wright ◽  
H. D. Colby ◽  
P. R. Miles
Keyword(s):  
Alveolar Macrophages ◽  
Membrane Surface ◽  
Lung Cells ◽  
Alveolar Type ◽  
Type Ii Cells ◽  
Type Ii ◽  
Sodium Influx ◽  
Saturation Kinetics ◽  
Ascorbate Uptake ◽  
Isolated Rat

Studies were conducted to measure intracellular ascorbate content and to characterize ascorbate uptake in three fractions of isolated rat pneumocytes (i.e., alveolar macrophages, alveolar type II epithelial cells, and another fraction of small pneumocytes that contains neither macrophages nor type II cells). When cells are incubated in medium containing 0.1 mM ascorbate (i.e., the concentration normally found in plasma), intracellular ascorbate concentrations are 3.2 mM in alveolar macrophages and type II cells and 0.9 mM in other lung cells; ascorbate influx is 1.5 nmol . 10(7) cells-1 . h-1 for alveolar macrophages, 0.24 nmol . 10(7) cells-1 . h-1 for type II cells, and very slow in other pneumocytes. Ascorbate influx displays saturation kinetics in both alveolar macrophages (K1/2 = 2 mM; Vmax = 32.2 nmol . 10(7) cells-1 . h-1) and type II cells (K1/2 = 5 mM; Vmax = 14.2 nmol . 10(7) cells-1 . h-1). After correction for differences in the membrane surface areas of these two types of lung cells, the rates for maximum ascorbate influx (Vmax) are similar in alveolar macrophages and type II cells. In addition, ascorbate uptake by alveolar macrophages and type II cells is dependent on metabolic activity and extracellular sodium. In contrast, ascorbate uptake in other lung cells does not exhibit saturation kinetics and is not dependent on metabolism or sodium. Thus alveolar macrophages and type II cells possess an energy-dependent cotransport system for ascorbate and sodium influx. The high ascorbate content and the existence of a specialized transport mechanism for ascorbate uptake may explain the relative resistance of alveolar macrophages and type II cells to oxidant injury.

Isolation of alveolar type II cells from fetal rat lung by differential adherence in monolayer culture

1988 ◽  
Vol 960 (3) ◽  
pp. 441-453 ◽  
Author(s):  
Joseph J. Batenburg ◽  
Caroline J.M. Otto-Verberne ◽  
Ank A.W. Ten Have-Opbroek ◽  
Wies Klazinga
Keyword(s):  
Monolayer Culture ◽  
Alveolar Type ◽  
Type Ii Cells ◽  
Type Ii ◽  
Rat Lung ◽  
Alveolar Type Ii Cells ◽  
Fetal Rat ◽  
Fetal Rat Lung

Effects of oligohydramnios on lung growth and maturation in the fetal rat

2002 ◽  
Vol 282 (3) ◽  
pp. L431-L439 ◽  
Author(s):  
Joseph A. Kitterman ◽  
Cheryl J. Chapin ◽  
Jeff N. Vanderbilt ◽  
Nicolas F. M. Porta ◽  
Louis M. Scavo ◽  
...  
Keyword(s):  
Fetal Lung ◽  
Alveolar Type ◽  
Type I ◽  
Type Ii Cells ◽  
Type Ii ◽  
Lung Growth ◽  
Type I Cells ◽  
Fetal Lung Development ◽  
Fetal Rat ◽  
I Cells

Oligohydramnios (OH) retards fetal lung growth by producing less lung distension than normal. To examine effects of decreased distension on fetal lung development, we produced OH in rats by puncture of uterus and fetal membranes at 16 days of gestation; fetuses were delivered at 21 or 22 days of gestation. Controls were position-matched littermates in the opposite uterine horn. OH lungs had lower weights and less DNA, protein, and water, but no differences in saturated phosphatidylcholine, surfactant proteins (SP)-A and -B, and mRNA for SP-A, -B, -C, and -D. To evaluate effects on epithelial differentiation, we used RTI40 and RTII70, proteins specific in lung to luminal surfaces of alveolar type I and II cells, respectively. At 22 days of gestation, OH lungs had less RTI40 mRNA ( P < 0.05) and protein ( P < 0.001), but RTII70 did not differ from controls. With OH, type I cells (in proportion to type II cells) covered less distal air space perimeter ( P < 0.01). We conclude that OH, which retards lung growth, has little effect on surfactant and impedes formation of type I cells relative to type II cells.

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