Regulation of Surfactant Secretion in Cultured Type II Cells1

2015 ◽  
pp. 115-121 ◽  
Author(s):  
L. G. Dobbs ◽  
H. R. W. Wirtz ◽  
M. S. Pian
Keyword(s):  
Type Ii ◽  
Surfactant Secretion

scholarly journals Pulmonary surfactant secretion in type II pneumocytes in the existence of inflammatory cells

1990 ◽  
Vol 52 ◽  
pp. 184
Author(s):  
Yoshiaki Oda ◽  
Hirofumi Kai ◽  
Kazunori Takaki ◽  
Tae Yasunaga ◽  
Kouichirou Murahara ◽  
...  
Keyword(s):  
Pulmonary Surfactant ◽  
Inflammatory Cells ◽  
Type Ii ◽  
Type Ii Pneumocytes ◽  
Surfactant Secretion

Activation of G proteins may inhibit or stimulate surfactant secretion in rat alveolar type II cells

1994 ◽  
Vol 266 (4) ◽  
pp. L375-L381 ◽  
Author(s):  
M. S. Pian ◽  
L. G. Dobbs
Keyword(s):  
G Proteins ◽  
Tonic Inhibition ◽  
Alveolar Type ◽  
Type Ii Cells ◽  
Type Ii ◽  
Alveolar Type Ii Cells ◽  
Intact Cells ◽  
Permeabilized Cells ◽  
Cyclic Monophosphate ◽  
Surfactant Secretion

To investigate how G proteins regulate surfactant secretion, we subjected rat alveolar type II cells to conditions known to activate or to inactivate G proteins. AlF-4, which activates G proteins, inhibited secretion in intact cells. Guanosine-5'-O-(3-thiotriphosphate), which activates G proteins in permeabilized cells, stimulated secretion at basal cytosolic [Ca2+], but inhibited secretion at higher [Ca2+]. In contrast, guanosine-5'-O-(2-thiodiphosphate) (GDP beta S), which inactivates G proteins, stimulated secretion at each [Ca2+] tested. Because treatment with GDP beta S stimulated secretion at basal cytosolic [Ca2+], surfactant secretion appears to be subject to G protein-regulated tonic inhibition. Pertussis toxin (PTX) inhibited terbutaline- and ionomycin-stimulated secretion in intact cells, but did not inhibit secretion stimulated by either forskolin or 8-bromoadenosine 3',5'-cyclic monophosphate. Inhibition by PTX of terbutaline-stimulated, but not 8-bromoadenosine 3',5'-cyclic monophosphate- or forskolin-stimulated secretion, suggests that PTX-sensitive G proteins regulate beta-adrenergic-stimulated surfactant secretion proximal to second messenger generation. Inhibition of ionomycin-stimulated secretion, however, suggests that PTX-sensitive G proteins may also regulate non-receptor-mediated secretory events.

Verapamil: a novel probe of surfactant secretion from rat type II pneumocytes

1989 ◽  
Vol 66 (3) ◽  
pp. 1304-1308 ◽  
Author(s):  
D. Warburton ◽  
L. Parton ◽  
S. Buckley ◽  
L. Cosico
Keyword(s):  
Inositol Phosphates ◽  
Calcium Influx ◽  
Concentration Effect ◽  
Type Ii ◽  
Calcium Efflux ◽  
Lactate Dehydrogenase Release ◽  
Type Ii Pneumocytes ◽  
Surfactant Secretion ◽  
Camp Formation ◽  
Stimulation Of

Surfactant from type II pneumocytes prevents the alveolar atelectasis found in both the neonatal and adult forms of respiratory distress syndrome. We have found that verapamil, a phenylalkene with calcium channel and alpha 1-receptor binding properties, has a multiphasic concentration effect on surfactant secretion from [3H]choline-labeled rat type II pneumocytes in culture. Verapamil (10(-8) M) caused a 24% stimulation of surfactant secretion, whereas an 8% inhibition was found at 10(-6) M and a 70% stimulation was found at 10(-4) M. Lactate dehydrogenase release occurred at 5 x 10(-4) M verapamil. Verapamil (10(-4) M) also produced a 100% increase in adenosine 3′5′-cyclic monophosphate (cAMP) in comparison with concentrations of less than or equal to 10(-6) M, an effect that could not be blocked by propranolol (10(-4) M). Verapamil (10(-6) M) increased the total formation of inositol phosphates (IP) by 23% in comparison with IP formation in control cells. Calcium influx was inhibited 15% by 10(-8) M verapamil and 37% by 10(-4) M verapamil. Calcium efflux was stimulated 44% by 10(-5) M verapamil. In combination with 50% effective concentrations (EC50) of terbutaline, phorbol ester, and ATP, the respective effects of verapamil (10(-4) M) on surfactant secretion were approximately additive. We conclude that verapamil has a novel multiphasic concentration effect on surfactant secretion, which appears to involve several signal transduction pathways including cAMP formation, IP formation, inhibition of calcium influx, and stimulation of calcium efflux.

scholarly journals MEMBRANE POTENTIAL RESPONSES OF TYPE II CELLS DURING SURFACTANT SECRETION

1984 ◽  
Vol 18 ◽  
pp. 391A-391A ◽  
Author(s):  
Jacob N Finkelstein ◽  
Richard L Gallo ◽  
Robert H Notter ◽  
Donald L Shapiro
Keyword(s):  
Membrane Potential ◽  
Type Ii Cells ◽  
Type Ii ◽  
Surfactant Secretion

Regulation of ATP-dependent surfactant secretion and activation of second-messenger systems in alveolar type II cells

1991 ◽  
Vol 261 (4) ◽  
pp. L105-L109
Author(s):  
T. A. Voyno-Yasenetskaya ◽  
L. G. Dobbs ◽  
M. C. Williams
Keyword(s):  
Protein Kinase C ◽  
Protein Kinase ◽  
Pertussis Toxin ◽  
Alveolar Type ◽  
Type Ii Cells ◽  
Type Ii ◽  
Calmodulin Antagonist ◽  
Pi Turnover ◽  
Kinase C ◽  
Surfactant Secretion

Several different classes of agonists are known to stimulate exocytosis in type II cells. These agonists cause increases in second messengers, such as adenosine 3',5'-cyclic monophosphate (cAMP) or cytosolic Ca2+, and/or stimulate protein kinase C. We studied generation of cAMP and phosphoinositide (PI) turnover in monolayer cultures of type II cells and measured [Ca2+]i in single cultured cells. ATP [10-4 M], which stimulates secretion of phosphatidylcholine (PC) and increases cellular cAMP, also stimulated PI turnover and increased [Ca2+]i. 12-O-tetradecanoylphorbol-13-acetate (TPA), which stimulates PC secretion and activates protein kinase C, did not increase [Ca2+]i. Pretreatment of type II cells with the calmodulin antagonist N-(6-aminohexyl)-5-chloro-1-naphthalenesulfonamide (W-7) inhibited the PC secretion induced by ATP and TPA and blocked the increase in PI turnover caused by ATP. ATP-dependent surfactant secretion and stimulation of PI turnover could also be inhibited by pretreatment of the cells with pertussis toxin. We used the fluorescent probe indo-1 to measure [Ca2+]i in single cultured type II cells. ATP produced rapid transient increases in [Ca2+]i, which could be prevented by pretreatment of the cells with either TPA or W-7. Our data suggest that pertussis toxin-sensitive G protein(s) are involved in ATP-dependent activation of PI turnover and in secretion of surfactant in type II cells. Activation of protein kinase C blocks the ATP-stimulated increase in [Ca2+]i. Finally, calmodulin may be involved in the regulation of ATP-dependent increase in [Ca2+]i, the activation of PI turnover, and the secretion of surfactant in type II cells. lung; exocytosis; cell calcium; G proteins; phosphoinositide turnover

Histamine stimulation of surfactant secretion from rat type II pneumocytes

1990 ◽  
Vol 258 (4) ◽  
pp. L195-L200 ◽  
Author(s):  
M. Chen ◽  
L. A. Brown
Keyword(s):  
Adenylate Cyclase ◽  
Receptor Antagonist ◽  
Maximal Response ◽  
Dependent Manner ◽  
Type Ii ◽  
Secretory Rate ◽  
Type Ii Pneumocytes ◽  
Adrenergic Antagonist ◽  
H2 Antagonist ◽  
Surfactant Secretion

The present study examined the effect of histamine on the secretion of phosphatidylcholine, the predominant component of pulmonary surfactant from adult rat alveolar type II pneumocytes in primary culture. Histamine stimulated surfactant secretion in a time- and dose-dependent manner. At a concentration of 10 microM, histamine stimulated surfactant release by 5.2-fold over the basal secretory rate. The concentration producing half the maximal response for histamine-induced secretion was 70 nM. Histamine-induced secretion was blocked by both the selective histamine1 receptor antagonist pyrilamine and the selective histamine2 receptor antagonist cimetidine, but not by the beta-adrenergic antagonist alprenolol. Histamine activated adenylate cyclase and intracellular adenosine 3',5'-cyclic monophosphate (cAMP) production. These effects on adenylate cyclase and cAMP induced by histamine were inhibited by the H2 antagonist cimetidine. This would suggest that surfactant secretion was stimulated by histamine through H2 receptors and by cAMP. When histamine and isoproterenol were added concomitantly, the effects on phosphatidylcholine secretion were additive; however, there was no additive effect on adenylate cyclase activation. This coupled with H2 antagonist pyrilamine inhibition of histamine-induced secretion would suggest that histamine stimulated surfactant secretion through another mechanism in addition to a cAMP-dependent mechanism.

scholarly journals Mechanical stretch activates piezo1 in caveolae of alveolar type I cells to trigger ATP release and paracrine stimulation of surfactant secretion from alveolar type II cells

2020 ◽  
Vol 34 (9) ◽  
pp. 12785-12804 ◽  
Author(s):  
Kathrin Diem ◽  
Michael Fauler ◽  
Giorgio Fois ◽  
Andreas Hellmann ◽  
Natalie Winokurow ◽  
...  
Keyword(s):  
Atp Release ◽  
Mechanical Stretch ◽  
Alveolar Type ◽  
Type I ◽  
Type Ii Cells ◽  
Type Ii ◽  
Alveolar Type Ii Cells ◽  
Surfactant Secretion ◽  
I Cells ◽  
Stimulation Of
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