scholarly journals IL-17A Recruits Rab35 to IL-17R to Mediate PKCα-Dependent Stress Fiber Formation and Airway Smooth Muscle Contractility

2019 ◽  
Vol 202 (5) ◽  
pp. 1540-1548 ◽  
Author(s):  
Katarzyna Bulek ◽  
Xing Chen ◽  
Vandy Parron ◽  
Aparna Sundaram ◽  
Tomasz Herjan ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Airway Smooth Muscle ◽  
Stress Fiber ◽  
Fiber Formation ◽  
Muscle Contractility ◽  
Smooth Muscle Contractility ◽  
Stress Fiber Formation

Carbachol-induced actin reorganization involves Gi activation of Rho in human airway smooth muscle cells

1998 ◽  
Vol 274 (5) ◽  
pp. L803-L809 ◽  
Author(s):  
Hideaki Togashi ◽  
Charles W. Emala ◽  
Ian P. Hall ◽  
Carol A. Hirshman
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Airway Smooth Muscle ◽  
Muscle Cells ◽  
Stress Fiber ◽  
Fiber Formation ◽  
Airway Smooth Muscle Cells ◽  
Human Airway Smooth Muscle ◽  
Human Airway ◽  
Stress Fiber Formation

To determine whether M2 muscarinic receptors are linked to the monomeric G protein Rho, we studied the effect of carbachol on actin reorganization (stress fiber formation) in cultured human airway smooth muscle cells that expressed mainly M2 muscarinic receptors by dual- fluorescence labeling of filamentous (F) and monomeric (G) actin. F-actin was labeled with FITC-labeled phalloidin, and G-actin was labeled with Texas Red-labeled DNase I. Carbachol stimulation induced stress fiber formation (increased F-actin staining) in the cells and increased the F- to G-actin ratio 3.6 ± 0.4-fold (mean ± SE; n = 5 experiments). Preincubation with pertussis toxin, Clostridium C3 exoenzyme, or tyrosine kinase inhibitors reduced the carbachol-induced increase in stress fiber formation and significantly decreased the F- to G-actin ratio, whereas a mitogen-activated protein kinase inhibitor, a phosphatidylinositol 3-kinase inhibitor, and a protein kinase C inhibitor were without effect. This study demonstrates that in cultured human airway smooth muscle cells, muscarinic-receptor activation induces stress fiber formation via a pathway involving a pertussis-sensitive G protein, Rho proteins, and tyrosine phosphorylation.

Gαi-2 is required for carbachol-induced stress fiber formation in human airway smooth muscle cells

1998 ◽  
Vol 275 (5) ◽  
pp. L911-L916 ◽  
Author(s):  
Carol A. Hirshman ◽  
Hideaki Togashi ◽  
Dan Shao ◽  
Charles W. Emala
Keyword(s):  
Smooth Muscle ◽  
G Protein ◽  
Airway Smooth Muscle ◽  
Muscarinic Receptors ◽  
Stress Fiber ◽  
Fiber Formation ◽  
Human Airway Smooth Muscle ◽  
Α Subunit ◽  
Human Airway ◽  
Stress Fiber Formation

To determine which heterotrimeric G protein couples muscarinic receptors to stress fiber formation [measured by an increase in the filamentous (F)- to monomeric (G)-actin ratio] in human airway smooth muscle (ASM) cells, cultured human ASM cells expressing the M2 muscarinic receptor were grown to confluence. Cells were exposed for 6 days to 10 μM antisense oligonucleotides designed to specifically bind to the mRNA encoding Gαi-2, Gαi-3, or Gqα. A randomly scrambled oligonucleotide served as a control. F- to G-actin ratios were measured with dual-fluorescence labeling after 5 min of carbachol exposure, which is known to increase the F- to G-actin ratio. Cells in parallel wells were harvested for immunoblot analysis of G protein α-subunit expression. Oligonucleotide antisense treatment decreased protein expression of the respective G protein α-subunit. Antisense depletion of the Gαi-2 protein but not of Gαi-3 or Gqα protein blocked the carbachol-induced increase in the F- to G-actin ratio. These results show that the Gαi-2 protein couples muscarinic receptors to stress fiber formation in ASM.

scholarly journals Prenatal Exposure to Respiratory Syncytial Virus Alters Postnatal Immunity and Airway Smooth Muscle Contractility during Early-Life Reinfections

PLoS ONE ◽  
2017 ◽  
Vol 12 (2) ◽  
pp. e0168786 ◽  
Author(s):  
Paul M. Brown ◽  
Terri J. Harford ◽  
Vandana Agrawal ◽  
Belinda Yen-Lieberman ◽  
Fariba Rezaee ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Respiratory Syncytial Virus ◽  
Airway Smooth Muscle ◽  
Prenatal Exposure ◽  
Early Life ◽  
Muscle Contractility ◽  
Smooth Muscle Contractility ◽  
Syncytial Virus
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