Integrin mediation of type II cell adherence to provisional matrix proteins

1996 ◽  
Vol 271 (2) ◽  
pp. L277-L286 ◽  
Author(s):  
H. J. Kim ◽  
D. H. Ingbar ◽  
C. A. Henke
Keyword(s):  
Cell Adhesion ◽  
Matrix Proteins ◽  
Alveolar Type ◽  
Type I ◽  
Type Ii Cells ◽  
Type Ii ◽  
Alveolar Cells ◽  
Type Ii Cell ◽  
Type Ii Alveolar Cells ◽  
Alpha V Beta 3

Lung injury causes alveolar type I epithelial cell death, basement membrane denudation, and alveolar flooding with serum fibronectin and fibrinogen. For successful restoration of normal architecture, the epithelium must be regenerated from progenitor type II alveolar cells. Using adhesion assays, we examined whether type II alveolar cells adhere to the provisional matrix proteins fibronectin, fibrinogen, and fibrin, and whether integrins mediate this adherence. Rat type II cells adhered to fibronectin, vitronectin, fibrinogen, and fibrin. Synthetic RGD (arginine-glycine-aspartic acid) peptide blocked this adhesion. Flow cytometry and Western analysis indicated that type II cells expressed beta 1- and alpha v beta 3-integrins. Anti-beta 1-and anti-alpha v beta 3-integrin antibodies blocked type II cell adhesion to fibronectin and to fibronectin and fibrinogen, respectively. In summary, type II cells adhered to fibronectin, fibrinogen, and fibrin, and adhesion was partially mediated by integrins. This study provides the first evidence of type II cell adhesion to fibrin gels and vitronectin, beta 1- and alpha v beta 3-integrin mediation of type II cell adhesion, and the presence of the alpha v beta 3-integrin on type II epithelial cells.

Sulfation of extracellular matrices modifies responses of alveolar type II cells to fibroblast growth factors

1996 ◽  
Vol 271 (5) ◽  
pp. L688-L697 ◽  
Author(s):  
P. L. Sannes ◽  
J. Khosla ◽  
P. W. Cheng
Keyword(s):  
Growth Factors ◽  
Biological Significance ◽  
Alveolar Type ◽  
Type I ◽  
Type Ii Cells ◽  
Type Ii ◽  
Fibroblast Growth ◽  
Alveolar Type Ii Cells ◽  
Proliferation And Differentiation ◽  
Type Ii Cell

The pulmonary alveolar basement membrane (BM) associated with alveolar type II cells has been shown to be significantly less sulfated than that of type I cells. To examine the biological significance of this observation, we measured the incorporation of 5-bromodeoxyuridine (BrdU) as an indicator of DNA synthesis in isolated rat type II cells cultured for 72-120 h on substrata that were naturally sulfated, not sulfated, or chemically desulfated in serum-free, hormonally defined media, with and without selected growth factors. The percentage of cells incorporating BrdU was significantly elevated by desulfated chondroitin sulfate in the presence of fibroblast growth factor-2 (FGF-2 or basic FGF) and depressed by heparin in the presence of either FGF-1 or acidic FGF or FGF-2. This depressive effect was lost by removing sulfate from the heparin. Some responses were dependent on the period of time in culture and concentration and molecular weight of the substrata. These observations support the notion that sulfation per se of certain components of BM is a key determinant of type II cell responses to select growth factors that may define patterns of proliferation and differentiation.

Alveolar type II cell growth on a pulmonary endothelial extracellular matrix

1996 ◽  
Vol 270 (6) ◽  
pp. L1017-L1022 ◽  
Author(s):  
I. Y. Adamson ◽  
L. Young
Keyword(s):  
Extracellular Matrix ◽  
Endothelial Cells ◽  
Cell Growth ◽  
Alveolar Type ◽  
Thymidine Uptake ◽  
Type I ◽  
Type Ii Cells ◽  
Type Ii ◽  
Lamellar Bodies ◽  
Type Ii Cell

Most of the alveolar epithelium overlies a fused basement membrane produced by epithelial and endothelial cells. To determine how this type of matrix influences type II cell growth and function, we studied the effects of culturing isolated rat alveolar type II cells on an extracellular matrix (ECM) freshly produced by pulmonary vascular endothelial cells grown 5 days in culture. Type II cells from the same rats were cultured on plastic or Matrigel for comparison. A large increase in mitotic activity was seen in type II cells grown on the endothelial ECM at 2 days only; thereafter cells spread rapidly to confluence and lost their lamellar bodies. Cells grown on Matrigel remained cuboidal with lamellar bodies but grew more slowly, as judged by [3H]thymidine uptake and cell numbers. Incorporation of labeled choline into disaturated phosphatidylcholine (DSPC) was used as a marker of surfactant synthesis. After the rapid, brief burst of proliferation, type II cells on endothelial ECM showed a sudden decline in DSPC-DNA by day 4 compared with cells grown on matrigel. Binding of the lectin Bauhinia purpurea (BPA) indicated that after a phase of division, cells on endothelial ECM developed as type I epithelium by 4 days of culture, when > 70% of cells stained positively for BPA binding, whereas few cuboidal cells on Matrigel were stained. The results indicate that type II cells respond briefly to growth factors in pulmonary endothelial ECM; then this type of matrix promotes cell spreading with loss of type II function as cells subsequently resemble type I epithelium.

In vivo exposure to hyperoxia induces DNA damage in a population of alveolar type II epithelial cells

2004 ◽  
Vol 286 (5) ◽  
pp. L1045-L1054 ◽  
Author(s):  
Jason M. Roper ◽  
Dawn J. Mazzatti ◽  
Richard H. Watkins ◽  
William M. Maniscalco ◽  
Peter C. Keng ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Transmembrane Protein ◽  
Dna Integrity ◽  
Alveolar Type ◽  
Type I ◽  
Type Ii Cells ◽  
Type Ii ◽  
Alveolar Cells ◽  
Endogenous Expression

It is well established that hyperoxia injures and kills alveolar endothelial and type I epithelial cells of the lung. Although type II epithelial cells remain morphologically intact, it remains unclear whether they are also damaged. DNA integrity was investigated in adult mice whose type II cells were identified by their endogenous expression of pro-surfactant protein C or transgenic expression of enhanced green fluorescent protein. In mice exposed to room air, punctate perinuclear 8-oxoguanine staining was detected in ∼4% of all alveolar cells and in 30% of type II cells. After 48 or 72 h of hyperoxia, 8-oxoguanine was detected in 11% of all alveolar cells and in >60% of type II cells. 8-Oxoguanine colocalized by confocal microscopy with the mitochondrial transmembrane protein cytochrome oxidase subunit 1. Type II cells isolated from hyperoxic lungs exhibited nuclear DNA strand breaks by comet assay even though they were viable and morphologically indistinguishable from cells isolated from lungs exposed to room air. These data reveal that type II cells exposed to in vivo hyperoxia have oxidized and fragmented DNA. Because type II cells are essential for lung remodeling, our findings raise the possibility that they are proficient in DNA repair.

Demonstration of Microtubules in Type II Alveolar Cells

1977 ◽  
Vol 35 ◽  
pp. 464-465
Author(s):  
Frederick J. Stone ◽  
Yutaka Kikkawa
Keyword(s):  
Secretory Granules ◽  
Alveolar Epithelial Cells ◽  
Type Ii Cells ◽  
Type Ii ◽  
Alveolar Cells ◽  
Alveolar Epithelial ◽  
Type Ii Cell ◽  
Type Ii Alveolar Cells ◽  
Probable Role ◽  
Secretory Products

Two lines of evidence indicate a probable role for microtubules in the secretory processes of type II alveolar epithelial cells. These are: (1) The inhibition of the release of disaturated lecithins (the major component of putative type II cell secretory products) by lung slices pretreated and then incubated with antimicrotubular agents colchicine and vinblastine (Delahunty, J.J. and Johnston, J.M.: J. Lipid Res., 17:112,1976); and (2) The abnormality of the secretory granules, lamellar bodies, in the type II cells of beige mice (Chi, E.Y. Prueitt, J.L., and Lagunoff, D: J. Histochem. Cytochem., 23:863-869, 1975) in which microtubular function is abnormal (Oliver, J.M.: Amer. J. Pathol., 85:395, 1976). Our failure to morphologically identify the expected microtubules in type II cells from lungs prepared for electron microscopy by conventional fixations led us to attempt their visualization by the application of the tannic acid- glutaraldehyde fixative of Futaesakie, et. al. (Histochemistry and Cytochemistry, 1972.).

Expression ofN-deacetylase/sulfotransferase and 3-O-sulfotransferase in rat alveolar type II cells

2000 ◽  
Vol 279 (2) ◽  
pp. L292-L301 ◽  
Author(s):  
Zhong-Yuan Li ◽  
Kazunori Hirayoshi ◽  
Yasuhiro Suzuki
Keyword(s):  
Heparan Sulfate ◽  
Protein A ◽  
Sodium Chlorate ◽  
Alveolar Type ◽  
Type I ◽  
Type Ii Cells ◽  
Type Ii ◽  
Type I Cells ◽  
Type Ii Cell ◽  
I Cells

Basal laminae beneath alveolar type I cells are suggested to contain highly sulfated heparan sulfate-containing proteoglycans (PGs), and cultured type II cells accumulate highly sulfated matrices. To characterize the regulation of PG synthesis during the transition from type II cells to type I cells, we examined mRNA expression of N-deacetylase/sulfotransferase (NST) and 3- O-sulfotransferase (3-OST), two enzymes specific for heparan sulfate synthesis. We found that both freshly isolated and cultured type II cells expressed NST and 3-OST as shown by in situ hybridization. Expression of surfactant-associated protein A, B, and C mRNAs, determined by semiquantitative PCR, decreased during culture. Expression of type I cell marker T1α mRNA increased except in cells cultured on an Engelbrecht-Holm-Swarm gel. Expression of NST was dependent on cell density and matrix and was intense in conditions where cells spread fully, whereas 3-OST expression was unchanged in the conditions examined. The PG sulfation inhibitor sodium chlorate significantly inhibited cultured type II cell spreading, and this inhibition was reversed by sodium sulfate. These results suggest that highly sulfated PGs modified by NST are necessary for the spreading of cells during transdifferentiation of type II cells to mature type I cells.

Alterations of type II cell microvilli following ozone-induced alveolar injury

1988 ◽  
Vol 46 ◽  
pp. 326-327
Author(s):  
E. M. Haller ◽  
J. F. Paterson ◽  
J. M. Lundh ◽  
J. U. Balis
Keyword(s):  
Left Lobe ◽  
Ozone Exposure ◽  
Male Rats ◽  
Alveolar Type ◽  
Type I ◽  
Type Ii Cells ◽  
Type Ii ◽  
Type Ii Cell ◽  
High Concentrations ◽  
Injury And Repair

Ozone is a major oxidizing constituent in photochemical smog, and it is known to cause, at high concentrations, bronchiolo-al veoar injury with early loss of cilia and desquamation of alveolar type I cells, followed by proliferation of type II cells. In the present study, we investigated the sequential sur face alterations of alveolar type II cells using an established model for ozone-induced alveolar injury and repair.Fisher 344 male rats weighing 260±10g were exposed to 3 ppm ozone for 8 h. The animals were killed at various time intervals, inclduing zero time, 24, 48, and 96 h after termination of ozone exposure. The lungs were inflated at 20cm pressure with 2.5% glutaraldehyde in 0.1M Sorensen's phosphate buffer, ph 7.2, at 37 C for 4 h. Lung slices, 10 x 4 mm x 500 μm, were obtained by random selection from the left lobe, osmicated in 1% phosphate buffered OsO4, for 1 h at 4 C, dehydrated in a graded series of acetone, infiltrated with Freon 113, and critical-point dried using carbon dioxide.

[Ca2+]i oscillations regulate type II cell exocytosis in the pulmonary alveolus

2000 ◽  
Vol 279 (1) ◽  
pp. L5-L13 ◽  
Author(s):  
Yugo Ashino ◽  
Xiaoyou Ying ◽  
Leland G. Dobbs ◽  
Jahar Bhattacharya
Keyword(s):  
Type I ◽  
Type Ii Cells ◽  
Type Ii ◽  
Alveolar Cells ◽  
Lung Inflation ◽  
Type I Cells ◽  
Lung Expansion ◽  
Type Ii Cell ◽  
I Cells

Pulmonary surfactant, a critical determinant of alveolar stability, is secreted by alveolar type II cells by exocytosis of lamellar bodies (LBs). To determine exocytosis mechanisms in situ, we imaged single alveolar cells from the isolated blood-perfused rat lung. We quantified cytosolic Ca2+ concentration ([Ca2+]i) by the fura 2 method and LB exocytosis as the loss of cell fluorescence of LysoTracker Green. We identified alveolar cell type by immunofluorescence in situ. A 15-s lung expansion induced synchronous [Ca2+]i oscillations in all alveolar cells and LB exocytosis in type II cells. The exocytosis rate correlated with the frequency of [Ca2+]i oscillations. Fluorescence of the lipidophilic dye FM1-43 indicated multiple exocytosis sites per cell. Intracellular Ca2+ chelation and gap junctional inhibition each blocked [Ca2+]i oscillations and exocytosis in type II cells. We demonstrated the feasibility of real-time quantifications in alveolar cells in situ. We conclude that in lung expansion, type II cell exocytosis is modulated by the frequency of intercellularly communicated [Ca2+]i oscillations that are likely to be initiated in type I cells. Thus during lung inflation, type I cells may act as alveolar mechanotransducers that regulate type II cell secretion.

scholarly journals Differential Response of Primary Alveolar Type I and Type II Cells to LPS Stimulation

PLoS ONE ◽  
2013 ◽  
Vol 8 (1) ◽  
pp. e55545 ◽  
Author(s):  
Mandi H. Wong ◽  
Meshell D. Johnson
Keyword(s):  
Differential Response ◽  
Alveolar Type ◽  
Type I ◽  
Type Ii Cells ◽  
Type Ii

Nitric oxide alters metabolism in isolated alveolar type II cells

1996 ◽  
Vol 271 (1) ◽  
pp. L23-L30 ◽  
Author(s):  
P. R. Miles ◽  
L. Bowman ◽  
L. Huffman
Keyword(s):  
Nitric Oxide ◽  
Oxygen Consumption ◽  
Atp Synthesis ◽  
Alveolar Type ◽  
Type Ii Cells ◽  
Type Ii ◽  
Atp Content ◽  
Alveolar Type Ii Cells ◽  
Type Ii Cell ◽  
Cellular Oxygen

Alveolar type II cells may be exposed to nitric oxide (.NO) from external sources, and these cells can also generate .NO. Therefore we studied the effects of altering .NO levels on various type II cell metabolic processes. Incubation of cells with the .NO generator, S-nitroso-N-acetylpenicillamine (SNAP; 1 mM), leads to reductions of 60-70% in the synthesis of disaturated phosphatidylcholines (DSPC) and cell ATP levels. Cellular oxygen consumption, an indirect measure of cell ATP synthesis, is also reduced by SNAP. There is no direct effect of SNAP on lung mitochondrial ATP synthesis, suggesting that .NO does not directly inhibit this process. On the other hand, incubation of cells with NG-nitro-L-arginine methyl ester (L-NAME), an inhibitor of nitric oxide synthase (NOS), the enzyme responsible for .NO synthesis, results in increases in DSPC synthesis, cell ATP content, and cellular oxygen consumption. The L-NAME effects are reversed by addition of L-arginine, the substrate for NOS. Production of .NO by type II cells is inhibited by L-NAME, a better inhibitor of constitutive NOS (cNOS) than inducible NOS (iNOS), and is reduced in the absence of external calcium. Aminoguanidine, a specific inhibitor of iNOS, has no effect on cell ATP content or on .NO production. These results indicate that alveolar type II cell lipid and energy metabolism can be affected by .NO and suggest that there may be cNOS activity in these cells.

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