Oxidants and antioxidants in alveolar epithelial type II cells: in situ, freshly isolated, and cultured cells

1992 ◽  
Vol 262 (1) ◽  
pp. L69-L77 ◽  
Author(s):  
V. L. Kinnula ◽  
L. Chang ◽  
J. I. Everitt ◽  
J. D. Crapo
Keyword(s):  
Superoxide Dismutase ◽  
Glutathione Reductase ◽  
Cultured Cells ◽  
Ex Vivo ◽  
Antioxidant Enzyme Activities ◽  
Type Ii Cells ◽  
Type Ii ◽  
Isolated Cells ◽  
Alveolar Epithelial

Antioxidant enzyme activities, H2O2 clearance, and H2O2 generation by rat alveolar epithelial type II cells were compared between in situ, freshly isolated (6 h ex vivo), and cultured cells (48 h ex vivo). Immunocytochemical studies did not show changes in catalase, Mn superoxide dismutase, or CuZn superoxide dismutase labeling density in cytoplasm, peroxisomes, or mitochondria. Numbers of peroxisomes and mitochondria per cell decreased in cultured cells. Biochemical studies showed that cell culture resulted in a significant decrease in activities of catalase (49%), glutathione reductase (50%), glutathione peroxidase (74%), and in the capacity of the cells to scavenge extracellular H2O2. Addition of the specific catalase inhibitor, aminotriazole, decreased the rate of consumption of exogenously added H2O2 in freshly isolated cells but not in cultured cells. Neither aminotriazole nor 1,3-bis (2-chloroethyl)-1-nitrosourea, which inactivates glutathione reductase, altered H2O2 consumption by cultured cells. The rate of extracellular H2O2 release in both freshly isolated and cultured cells was 0.71 nmol.min-1.mg protein-1. It can be concluded that levels of some antioxidant enzymes fall in cultured alveolar epithelial type II cells, and that, although catalase likely plays a significant role in protection of freshly isolated cells against oxidant stress, this pathway may be less important after culture.

pH-induced calcium transients in type II alveolar epithelial cells

1993 ◽  
Vol 264 (5) ◽  
pp. L448-L457 ◽  
Author(s):  
G. D. Gerboth ◽  
R. M. Effros ◽  
R. J. Roman ◽  
E. R. Jacobs
Keyword(s):  
Epithelial Cells ◽  
Fluorescent Dyes ◽  
Cultured Cells ◽  
Alveolar Epithelial Cells ◽  
Metabolic Effects ◽  
Type Ii Cells ◽  
Type Ii ◽  
Intracellular Acidification ◽  
Isolated Cells ◽  
Alveolar Epithelial

Although both intracellular pH (pHi) and intracellular Ca2+ concentration ([Ca2+]i) are highly regulated and have important metabolic effects in alveolar epithelial cells, little is known about the interrelationship between these two ions in alveolar epithelial cells. The present study examined changes in [pH]i and [Ca2+]i in isolated alveolar epithelial cells using the fluorescent dyes SNARF-1 and fura-2. Basal pHi values in freshly isolated and cultured alveolar epithelial cells were 7.27 and 7.24, respectively. Resting [Ca2+]i values in freshly isolated cells (53 +/- 5 nM) were lower than those in cultured type II cells (107 +/- 21 nM). pHi increased rapidly after addition of 25 mM NH4Cl in both cultured and freshly isolated cells and then decreased back toward baseline over the following 10 min. The rise in pHi was associated with a transient increase in [Ca2+]i. Resuspension of cells in an NH4Cl-free solution resulted in rapid intracellular acidification, which recovered over the subsequent 10 min. Removal of sodium or addition of 1 mM amiloride to the external solution slowed the rate of recovery from intracellular acidification, consistent with the participation of Na(+)-H+ exchanger in this process. In freshly isolated cells, [Ca2+]i increased following acidification and then decreased as the cells recovered from an acid load. In cultured cells, [Ca2+]i also increased following acidification but then remained elevated over the subsequent 10 min. The recovery of [Ca2+]i toward baseline values in fresh cells following acidification was dependent on the presence of external sodium. These data demonstrate that both increases and decreases in pHi of alveolar epithelial cells are associated with increases in [Ca2+]i and suggest that some of the metabolic effects of altering pHi may be secondary to increases in [Ca2+]i. The dependency of [Ca2+]i recovery following acidification on external sodium raises the possibility that freshly isolated type II cells have Na(+)-Ca2+ exchangers that contribute to the regulation of [Ca2+]i.

Disparate cytokine regulation of ICAM-1 in rat alveolar epithelial cells and pulmonary endothelial cells in vitro

1995 ◽  
Vol 269 (1) ◽  
pp. L127-L135 ◽  
Author(s):  
W. W. Barton ◽  
S. Wilcoxen ◽  
P. J. Christensen ◽  
R. Paine
Keyword(s):  
Endothelial Cells ◽  
Epithelial Cells ◽  
Inflammatory Cytokines ◽  
Alveolar Epithelial Cells ◽  
Normal Lung ◽  
Type I ◽  
Type Ii Cells ◽  
Type Ii ◽  
Alveolar Epithelial

Intercellular adhesion molecule-1 (ICAM-1) is expressed at high levels on type I alveolar epithelial cells in the normal lung and is induced in vitro as type II cells spread in primary culture. In contrast, in most nonhematopoetic cells ICAM-1 expression is induced in response to inflammatory cytokines. We have formed the hypothesis that the signals that control ICAM-1 expression in alveolar epithelial cells are fundamentally different from those controlling expression in most other cells. To test this hypothesis, we have investigated the influence of inflammatory cytokines on ICAM-1 expression in isolated type II cells that have spread in culture and compared this response to that of rat pulmonary artery endothelial cells (RPAEC). ICAM-1 protein, determined both by a cell-based enzyme-linked immunosorbent assay and by Western blot analysis, and mRNA were minimally expressed in unstimulated RPAEC but were significantly induced in a time- and dose-dependent manner by treatment with tumor necrosis factor-alpha, interleukin-1 beta, or interferon-gamma. In contrast, these cytokines did not influence the constitutive high level ICAM-1 protein expression in alveolar epithelial cells and only minimally affected steady-state mRNA levels. ICAM-1 mRNA half-life, measured in the presence of actinomycin D, was relatively long at 7 h in alveolar epithelial cells and 4 h in RPAEC. The striking lack of response of ICAM-1 expression by alveolar epithelial cells to inflammatory cytokines is in contrast to virtually all other epithelial cells studied to date and supports the hypothesis that ICAM-1 expression by these cells is a function of cellular differentiation.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals A Site-Specific Genetic Modification for Induction of Pluripotency and Subsequent Isolation of Derived Lung Alveolar Epithelial Type II Cells

Stem Cells ◽  
2014 ◽  
Vol 32 (2) ◽  
pp. 402-413 ◽  
Author(s):  
Qing Yan ◽  
Yuan Quan ◽  
Huanhuan Sun ◽  
Xinmiao Peng ◽  
Zhengyun Zou ◽  
...  
Keyword(s):  
Genetic Modification ◽  
Type Ii Cells ◽  
Type Ii ◽  
Site Specific ◽  
Alveolar Epithelial ◽  
A Site

Secretion of cytokines by rat alveolar epithelial cells: possible regulatory role for SP-A

1994 ◽  
Vol 266 (2) ◽  
pp. L148-L155 ◽  
Author(s):  
H. Blau ◽  
S. Riklis ◽  
V. Kravtsov ◽  
M. Kalina
Keyword(s):  
Epithelial Cells ◽  
Alveolar Epithelial Cells ◽  
Alveolar Type ◽  
Type Ii Cells ◽  
Type Ii ◽  
Alveolar Type Ii Cells ◽  
Long Term Culture ◽  
Alveolar Epithelial ◽  
Gm Csf

Cultured alveolar type II cells and pulmonary epithelial (PE) cells in long-term culture were found to secrete colony-stimulating factors (CSF) into the medium in similar fashion to alveolar macrophages. CSF activity was determined by using the in vitro assay for myeloid progenitor cells [colony-forming units in culture (CFU-C)]. Both lipopolisaccharide (LPS) and interleukin-1 alpha (IL-1 alpha) were found to upregulate the secretion 6.5- to 8-fold from alveolar type II cells and macrophages. However, no stimulatory effect of these factors was observed in PE cells that release CSF into the medium constitutively, possibly due to the conditions of long-term culture. The CSF activity was partially neutralized (70% inhibition) by antibodies against murine granulocyte/macrophage (GM)-CSF and IL-3, thus indicating the presence of both GM-CSF and IL-3-like factors in the CSF. However, the presence of other cytokines in the CSF is highly probable. Surfactant-associated protein A (SP-A), which is known to play a central role in surfactant homeostasis and function, was also found to upregulate secretion of CSF (at concentrations of 0.1-5 micrograms/ml) from alveolar type II cells and macrophages. Control cells such as rat peritoneal macrophages, alveolar fibroblasts, and 3T3/NIH cell line could not be elicited by SP-A to release CSF. The results are discussed in relation to the possible participation of the alveolar epithelial cells in various intercellular signaling networks. Our studies suggest that alveolar type II cells and SP-A may play an important regulatory role in the modulation of immune and inflammatory effector cells within the alveolar space.

scholarly journals The plate body: 3D ultrastructure of a facultative organelle of alveolar epithelial type II cells involved in SP-A trafficking

2020 ◽  
Author(s):  
Christian Mühlfeld ◽  
Christoph Wrede ◽  
Viktor Molnár ◽  
Alexandra Rajces ◽  
Christina Brandenberger
Keyword(s):  
Type Ii Cells ◽  
Type Ii ◽  
Alveolar Epithelial

Cyclic deformation-induced injury and differentiation of rat alveolar epithelial type II cells

2012 ◽  
Vol 180 (2-3) ◽  
pp. 237-246 ◽  
Author(s):  
Huan Ye ◽  
Qingyuan Zhan ◽  
Yanhong Ren ◽  
Xiaoyang Liu ◽  
Chun Yang ◽  
...  
Keyword(s):  
Cyclic Deformation ◽  
Type Ii Cells ◽  
Type Ii ◽  
Alveolar Epithelial
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