scholarly journals Postnatal development and control of the pulmonary surfactant system in the tammar wallaby Macropus eugenii

2001 ◽  
Vol 204 (23) ◽  
pp. 4031-4042
Author(s):  
Natalie J. Miller ◽  
Sandra Orgeig ◽  
Christopher B. Daniels ◽  
Russell V. Baudinette
Keyword(s):  
Gas Exchange ◽  
Pulmonary Surfactant ◽  
Tammar Wallaby ◽  
Surfactant Proteins ◽  
Alveolar Type ◽  
Type Ii Cells ◽  
Type Ii ◽  
Alveolar Type Ii Cells ◽  
Macropus Eugenii ◽  
Surfactant System

SUMMARY Marsupials are born at an early stage of development and are adapted for future development inside the pouch. Whether the pulmonary surfactant system is fully established at this altricial stage is unknown. This study correlates the presence of surfactant proteins (SP-A, SP-B and SP-D), using immunohistochemistry, with the ex-utero development of the lung in the tammar wallaby Macropus eugenii and also investigates the control of phosphatidylcholine (PC) secretion from developing alveolar type II cells. All three surfactant proteins were found at the site of gas exchange in the lungs of joeys at all ages, even at birth when the lungs are in the early stages of the terminal air-sac phase. Co-cultures of alveolar type II cells and fibroblasts were isolated from the lungs of 30- and 70-day-old joeys and incubated with the hormones dexamethasone (10 μmol l–1), prolactin (1 μmol l–1) or triiodothyronine (100 μmol l–1) or with the autonomic secretagogues isoproterenol (100 μmol l–1) or carbamylcholine chloride (100 μmol l–1). Basal secretion of PC was greater at 30 days of age than at 70 days. Co-cultures responded to all five agonists at 30 days of age, but only the autonomic secretagogues caused a significant increase in PC secretion at 70 days of age. This demonstrates that, as the cells mature, their activity and responsiveness are reduced. The presence of the surfactant proteins at the site of gas exchange at birth suggests that the system is fully functional. It appears that surfactant development is coupled with the terminal air-sac phase of lung development rather than with birth, the length of gestation or the onset of air-breathing.

Biosynthetic routing of pulmonary surfactant proteins in alveolar type II cells

1993 ◽  
Vol 26 (5) ◽  
pp. 366-373 ◽  
Author(s):  
W. F. Voorhout ◽  
T. E. Weaver ◽  
H. P. Haagsman ◽  
H. J. Geuze ◽  
L. M. G. Van Golde
Keyword(s):  
Pulmonary Surfactant ◽  
Surfactant Proteins ◽  
Alveolar Type ◽  
Type Ii Cells ◽  
Type Ii ◽  
Alveolar Type Ii Cells ◽  
Pulmonary Surfactant Proteins

Keratinocyte growth factor increases mRNAs for SP-A and SP-B in adult rat alveolar type II cells in culture

1995 ◽  
Vol 269 (3) ◽  
pp. L344-L350 ◽  
Author(s):  
K. Sugahara ◽  
J. S. Rubin ◽  
R. J. Mason ◽  
E. L. Aronsen ◽  
J. M. Shannon
Keyword(s):  
Growth Factors ◽  
Growth Factor ◽  
Keratinocyte Growth Factor ◽  
Primary Cultures ◽  
Surfactant Proteins ◽  
Alveolar Type ◽  
Type Ii Cells ◽  
Type Ii ◽  
Alveolar Type Ii Cells ◽  
Adult Rat

The production of pulmonary surfactant, a complex of phospholipids and lung-specific surfactant proteins, is a primary function of alveolar type II cells. Although previous studies have demonstrated a role for cell-extracellular matrix interactions and normal cell shape in the maintenance of differentiated function in primary cultures of adult rat type II cells, a positive role for growth factors in surfactant protein gene expression in isolated normal adult type II cells has not been reported. In the present study, we have examined the effects of a panel of hormones, growth factors, and cytokines on the expression of mRNAs for surfactant proteins A, B, and C (SP-A, SP-B, and SP-C). Our results show that keratinocyte growth factor (KGF) induced a two- to threefold increase in steady-state levels of mRNAs for SP-A and SP-B, but had no effect on or decreased SP-C mRNA. The increase in SP-A mRNA was accompanied by an increase in SP-A protein. The effects of KGF were both dose and time dependent, and they could be neutralized by a monoclonal antibody against KGF. The effects of KGF were mimicked by acidic fibroblast growth factor, which will bind the KGF receptor. We conclude that KGF can support differentiation of alveolar type II cells as well as act as a mitogen, thus suggesting an important role for KGF in maintenance of the alveolar epithelium.

Role of Peripheral Benzodiazepine Receptors on Secretion of Surfactant in Guinea Pig Alveolar Type II Cells

1999 ◽  
Vol 19 (5) ◽  
pp. 461-471 ◽  
Author(s):  
Salil K. Das ◽  
Shyamali Mukherjee
Keyword(s):  
Pulmonary Surfactant ◽  
Benzodiazepine Receptors ◽  
Alveolar Epithelium ◽  
Alveolar Type ◽  
Type Ii Cells ◽  
Type Ii ◽  
Alveolar Type Ii Cells ◽  
Peripheral Tissues ◽  
Dipalmitoyl Phosphatidylcholine ◽  
Peripheral Benzodiazepine Receptors

Granular type II cells located in the alveolar epithelium synthesize and secrete pulmonary surfactant and have specialized ion transport system. Alveolar type II cells are stimulated to secrete pulmonary surfactant by a variety of agonists. One mechanism by which extracellular signals are perceived by cells is the mobilization of intracellular Ca2+. Peripheral benzodiazepine receptors (PBRs) are present in both peripheral tissues and central nervous system. We have previously reported the presence of high density PBRs in lung and alveolar type II cells. It is known that both PBRs and beta-adrenergic receptors (beta-ARs) play an important role in cellular Ca2+ transport. Furthermore, we have suggested earlier that PBRs are someway functionally associated with the beta-ARs. The objective of the present study was to determine whether PBRs play any role in the secretion of surfactant by alveolar type II cells. Alveolar type II cells were isolated from normal weanling guinea pigs by panning method and incubated with 3H-palmitic acid in minimum essential medium to synthesize labelled dipalmitoyl phosphatidylcholine (DPPC). After washing, the cells were treated at 37°C for one hour with 10 μM isoproterenol (IP) in the presence and absence of 10 μM Ro 5-4864, an agonist for PBRs. After one hour, the release of labelled DPPC in the medium was analyzed. The control cells released DPPC without any addition of a ligand. However, the treatment of cells with IP, Ro 5-4864 and IP + Ro 5-4864 caused 24, 52 and 171% increase in the secretion of DPPC, respectively. In another experiment, type II cells were loaded with Fura-2 dye and treated with either IP or epineprine or Ro 5-4864. Both isoproterenol and epinephrine caused a significant increase in the level of cytosolic free Ca2+. However, Ro 5-4864 caused not only a decrease in the level of cytosolic free Ca2+ but also counteracted the stimulatory effect of IP. This may suggest that while ligands for ARs stimulate Ca2+ release into cytosol, the ligand for PBRs stimulates efflux of Ca2+ in alveolar type cells. Thus, the increased secretion of surfactant by the ligand of PBRs in alveolar type II cells may be mediated through its effects on increased Ca2+ efflux.

Effect of secretagogues on cytoplasmic free calcium in alveolar type II epithelial cells

1987 ◽  
Vol 253 (5) ◽  
pp. C679-C686 ◽  
Author(s):  
K. Sano ◽  
D. R. Voelker ◽  
R. J. Mason
Keyword(s):  
Pulmonary Surfactant ◽  
Calcium Concentration ◽  
Free Calcium ◽  
Alveolar Type ◽  
Type Ii Cells ◽  
Type Ii ◽  
Alveolar Type Ii Cells ◽  
Surfactant Secretion ◽  
Free Calcium Concentration ◽  
Cytoplasmic Free Calcium

Pulmonary surfactant is synthesized and secreted by alveolar type II epithelial cells. Although intracellular calcium and other second messengers have been implicated in secretion by type II cells, this is the first report on measurement of cytoplasmic free calcium concentration ([Ca2+]i). Known secretagogues, 12-O-tetradecanoylphorbol-13-acetate (TPA) and terbutaline, were tested to see if they caused rapid increases in cytoplasmic calcium. Ionomycin, a calcium ionophore, was used to increase cytoplasmic free calcium concentration, to determine if a rapid increase in cytoplasmic free calcium would stimulate secretion, and to measure interactions with other secretagogues. Ionomycin increased both [Ca2+]i and pulmonary surfactant secretion from alveolar type II cells. A low concentration of ionomycin (100 nM) greatly enhanced secretion stimulated by terbutaline or by 8-bromo-cAMP but only had an additive effect on secretion stimulated by TPA. Terbutaline transiently increased [Ca2+]i by 24% over control basal condition, and the increase in [Ca2+]i produced by terbutaline occurred in the absence of extracellular calcium. TPA itself did not change [Ca2+]i. However, TPA completely inhibited the terbutaline-induced increase of [Ca2+]i but not the increase due to ionomycin. When alveolar type II cells were loaded with 2-(2-bis-[carboxymethyl]-amino-5-methyl-phenoxy)-methyl-6-methoxy-8-bis carboxymethylaminoquinoline (quin2) in calcium-free buffer, [Ca2+]i decreased from 143 +/- 10 to 31 +/- 8 nM. Lowering [Ca2+]i inhibited TPA- or terbutaline-induced secretion by 22 and 40%, respectively. Although the precise role of cytoplasmic free calcium on surfactant secretion cannot be established on the basis of current data, our results indicate that an increase in cytoplasmic free calcium produced by ionomycin stimulates secretion and that an increase in [Ca2+]i affects cAMP-induced secretion more than protein kinase C-mediated secretion in alveolar type II cells.

scholarly journals Pulmonary Surfactant Preserves Viability of Alveolar Type II Cells Exposed to Polymyxin B In Vitro

PLoS ONE ◽  
2013 ◽  
Vol 8 (4) ◽  
pp. e62105 ◽  
Author(s):  
Guido Stichtenoth ◽  
Egbert Herting ◽  
Mario Rüdiger ◽  
Andreas Wemhöner
Keyword(s):  
Pulmonary Surfactant ◽  
Polymyxin B ◽  
Alveolar Type ◽  
Type Ii Cells ◽  
Type Ii ◽  
Alveolar Type Ii Cells

scholarly journals Pulmonary surfactant and its components inhibit secretion of phosphatidylcholine from cultured rat alveolar type II cells.

1987 ◽  
Vol 84 (4) ◽  
pp. 1010-1014 ◽  
Author(s):  
L. G. Dobbs ◽  
J. R. Wright ◽  
S. Hawgood ◽  
R. Gonzalez ◽  
K. Venstrom ◽  
...  
Keyword(s):  
Pulmonary Surfactant ◽  
Alveolar Type ◽  
Type Ii Cells ◽  
Type Ii ◽  
Alveolar Type Ii Cells
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