The role of calcium in the secretion of surfactant by rat alveolar type II cells

Dobbs, Leland G.; Gonzalez, Robert; Marinari, Lawrence A.; Mescher, E. Joseph; Hawgood, Samuel

doi:10.1016/0005-2760(86)90308-5

Cited by 64 publications

(24 citation statements)

References 32 publications

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“…The actions of ATP are more complex and involve both P 1 receptor-dependent cAMP formation (14) as well as P 2 receptor-dependent phosphoinositide hydrolysis and subsequent Ca 2ϩ mobilization (15)(16)(17). The actions of Ca 2ϩ and PKC and those of cAMP are additive, supporting the notion that surfactant secretion is independently regulated at various sites (18,19).…”

mentioning

confidence: 61%

Dynamics of surfactant release in alveolar type II cells

Haller

Ortmayr

Friedrich

et al. 1998

Proc. Natl. Acad. Sci. U.S.A.

138

182

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Pulmonary surfactant, secreted via exocytosis of lamellar bodies (LB) by alveolar type II (AT II) cells, maintains low alveolar surface tension and is therefore essential for normal lung function. Here we describe real-time monitoring of exocytotic activity in these cells by visualizing and quantifying LB fusion with the plasma membrane (PM). Two approaches were used. First, f luorescence of LysoTracker Green DND-26 (LTG) in LB disappeared when the dye was released after exocytosis. Second, phospholipid staining by FM 1-43 resulted in bright f luorescence when this dye entered the LB through the fusion pore. Both processes were restricted to and colocalized with LB and occurred simultaneously. In AT II cells, FM 1-43 offered the unique advantage to independently define the moment and cellular location of single exocytotic events as well as the amount of material released, and to monitor its extracellular fate. Furthermore, both dyes could be used in combination with fura-2. The results indicate considerable diversity in the dynamics of LB exocytosis. In the majority of cells stimulated with ATP and isoproterenol, the first fusion of LB coincided with the rise of [Ca 2؉ ] i , but subsequent response of other LB in the same cell considerably outlasted this signal. In other cells, however, the onset of exocytosis was delayed by several minutes. After LB fusion, release of surfactant from LB into an aqueous solution was slow. In summary, stimulated exocytosis in AT II cells occurs at a much slower rate than in most other secretory cells but is still a more dynamic process than predicted from conventional measurements of surfactant released into cell supernatants.

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mentioning

confidence: 61%

Dynamics of surfactant release in alveolar type II cells

Haller

Ortmayr

Friedrich

et al. 1998

Proc. Natl. Acad. Sci. U.S.A.

138

182

View full text Add to dashboard Cite

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“…Cell viability was measured by the exclusion of the vital dye, Trypan Blue (Dobbs et al, 1986b) using a haemocytometer (Neubauer improved, depth 0.1·mm, 0.0025·mm 2 ). Viable type II cells actively exclude the Trypan Blue dye and remain clear.…”

Section: Isolation Of Type II Cellsmentioning

confidence: 99%

Thermal acclimation of surfactant secretion and its regulation by adrenergic and cholinergic agonists in type II cells isolated from warm-active and torpid golden-mantled ground squirrels,Spermophilus lateralis

Ormond

Orgeig

Daniels

et al. 2003

Journal of Experimental Biology

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SUMMARYHomeothermic mammals experience pulmonary surfactant dysfunction with relatively small fluctuations in body temperature. However, ground squirrels survive dramatic changes in body temperature during hibernation, when body temperature drops from 37°C to 0-5°C during prolonged torpor bouts. Using type II cells isolated from both warm-active and torpid squirrels, we determined the effect of assay temperature, autonomic agonists and torpor on surfactant secretion. Basal secretion was significantly higher in type II cells isolated from torpid squirrels compared with warm-active squirrels when assayed at the body temperature of the animal from which they were isolated(4°C and 37°C, respectively). A change in assay temperature significantly decreased surfactant secretion. However, the change in secretory rate between 37°C and 4°C was less than expected if due to temperature alone (Q10 range=0.8-1.2). Therefore, the surfactant secretory pathway in squirrel type II cells demonstrates some temperature insensitivity. When incubated at the body temperature of the animal from which the cells were isolated, the adrenergic agonist, isoproterenol, significantly increased surfactant secretion in both warm-active and torpid squirrel type II cells. However, the cholinergic agonist, carbamylcholine chloride, only increased secretion in torpid squirrel type II cells when incubated at 4°C. Torpor did not affect basal cAMP production from isolated type II cells. However, the production of cAMP appears to be upregulated in response to isoproterenol in torpid squirrel type II cells. Thus, at the cellular level, both the secretory and regulatory pathways involved in surfactant secretion are thermally insensitive. Upregulating basal secretion and increasing the sensitivity of type II cells to cholinergic stimulation may be adaptative characteristics of torpor that enable type II cells to function effectively at 0-5°C.

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“…The existence of calcium-regulated pathways for surfactant secretion stems from a large body of pharmacological evidence obtained from primary type II cells in culture. Increases in intracellular calcium increase surfactant secretion either by a direct effect on the secretory machinery (70,75,109,117,242,316) or through a protein kinase C-dependent pathway (44,108,224,229,286), or both. Stimulation of surfactant secretion by endothelin-1 also shows both a calcium-and protein kinase C-dependent component (244).…”

Section: Calcium Transients and Heterocellular Regulation Of Surfactamentioning

confidence: 99%

Sharing signals: connecting lung epithelial cells with gap junction channels

Koval

2002

American Journal of Physiology-Lung Cellular and Molecular Phys

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Gap junction channels enable the direct flow of signaling molecules and metabolites between cells. Alveolar epithelial cells show great variability in the expression of gap junction proteins (connexins) as a function of cell phenotype and cell state. Differential connexin expression and control by alveolar epithelial cells have the potential to enable these cells to regulate the extent of intercellular coupling in response to cell stress and to regulate surfactant secretion. However, defining the precise signals transmitted through gap junction channels and the cross talk between gap junctions and other signaling pathways has proven difficult. Insights from what is known about roles for gap junctions in other systems in the context of the connexin expression pattern by lung cells can be used to predict potential roles for gap junctional communication between alveolar epithelial cells.

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The role of calcium in the secretion of surfactant by rat alveolar type II cells

Cited by 64 publications

References 32 publications

Dynamics of surfactant release in alveolar type II cells

Dynamics of surfactant release in alveolar type II cells

Thermal acclimation of surfactant secretion and its regulation by adrenergic and cholinergic agonists in type II cells isolated from warm-active and torpid golden-mantled ground squirrels,Spermophilus lateralis

Sharing signals: connecting lung epithelial cells with gap junction channels

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