scholarly journals Knockdown of flotillin-2 inhibits lung surfactant secretion by alveolar type II cells

Cell Research ◽  
2008 ◽  
Vol 18 (6) ◽  
pp. 701-703 ◽  
Author(s):  
Narendranath Reddy Chintagari ◽  
Deming Gou ◽  
Lin Liu
Keyword(s):  
Lung Surfactant ◽  
Alveolar Type ◽  
Type Ii Cells ◽  
Type Ii ◽  
Alveolar Type Ii Cells ◽  
Surfactant Secretion

Stimulation of lung surfactant secretion by endothelin-1 from rat alveolar type II cells

1994 ◽  
Vol 266 (3) ◽  
pp. L255-L262 ◽  
Author(s):  
N. Sen ◽  
M. M. Grunstein ◽  
A. Chander
Keyword(s):  
Endothelial Cells ◽  
Protein Kinase C ◽  
Protein Kinase ◽  
Lung Surfactant ◽  
Alveolar Type ◽  
Type Ii Cells ◽  
Type Ii ◽  
Alveolar Type Ii Cells ◽  
Kinase C ◽  
Surfactant Secretion

Endothelin-1 (ET-1), a potent vasoactive peptide released by endothelial cells, alters cytosolic Ca2+ and phosphoinositide metabolism in cells of myogenic and nonmyogenic origin. We evaluated the effect of ET-1 on surfactant phosphatidylcholine (PC) secretion from alveolar type II cells labeled with [methyl-3H]choline. ET-1 stimulated the secretion of PC in a time- and dose-dependent manner. Binding of 125I-labeled ET-1 to type II cell membranes was saturable at approximately 1 nM and suggested the presence of a single type of receptor. The secretagogue effect of ET-1 was independently inhibited by nifedipine and nitrendipine, both L-type calcium channel blockers, and removal of extracellular calcium. ET-1 also increased cellular diacylglycerol content by approximately 50% within 30 s, which could not be attenuated by pretreatment with nifedipine, suggesting an early activation of protein kinase C that was independent of Ca2+ influx. Further, ET-1-stimulated PC secretion was also blocked by inhibitors of protein kinase C. Collectively, these results indicate that the binding of ET-1 to type II cells is coupled to the activation of protein kinase C, which increases calcium influx through L-type calcium channels, and results in increased secretion of lung surfactant. Since ET-1 is released from pulmonary micro- and macrovasculature endothelial cells in close proximity to type II cells, our findings support the novel concept that endothelial cells interact with alveolar type II cells in a paracrine fashion to regulate 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.

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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