Effect of cigarette smoke extract on the role of protein kinase C in the proliferation of passively sensitized human airway smooth muscle cells

2005 ◽  
Vol 25 (3) ◽  
pp. 269-273 ◽  
Author(s):  
Lin Junling ◽  
Xu Yongjian ◽  
Zhang Zhenxiang ◽  
Ni Wang ◽  
Chen Shixin
Keyword(s):  
Smooth Muscle ◽  
Protein Kinase C ◽  
Protein Kinase ◽  
Smooth Muscle Cells ◽  
Cigarette Smoke ◽  
Cigarette Smoke Extract ◽  
Airway Smooth Muscle Cells ◽  
Human Airway Smooth Muscle ◽  
Kinase C

scholarly journals Phosphorylation of Kv7 potassium channels by protein kinase C in human airway smooth muscle cells

2013 ◽  
Vol 27 (S1) ◽  
Author(s):  
Jennifer M Haick ◽  
Lioubov I Brueggemann ◽  
Jeffrey R Prochot ◽  
Devjit S Randhawa ◽  
Christopher Wigfield ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Protein Kinase C ◽  
Protein Kinase ◽  
Potassium Channels ◽  
Smooth Muscle Cells ◽  
Airway Smooth Muscle ◽  
Muscle Cells ◽  
Airway Smooth Muscle Cells ◽  
Human Airway Smooth Muscle ◽  
Kinase C

Protein kinase C‐ε mediates bradykinin‐induced cyclooxygenase‐2 expression in human airway smooth muscle cells

2002 ◽  
Vol 16 (11) ◽  
pp. 1435-1437 ◽  
Author(s):  
Linhua Pang ◽  
Mei Nie ◽  
Lisa Corbett ◽  
Richard Donnelly ◽  
Samuel Gray ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Protein Kinase C ◽  
Protein Kinase ◽  
Smooth Muscle Cells ◽  
Airway Smooth Muscle ◽  
Muscle Cells ◽  
Airway Smooth Muscle Cells ◽  
Human Airway Smooth Muscle ◽  
Human Airway ◽  
Kinase C

scholarly journals An Antisense of Protein Kinase C- ζ Inhibits Proliferation of Human Airway Smooth Muscle Cells

2000 ◽  
Vol 23 (4) ◽  
pp. 555-559 ◽  
Author(s):  
Stephen Carlin ◽  
Philip Poronnik ◽  
David I. Cook ◽  
Lee Carpenter ◽  
Trevor J. Biden ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Protein Kinase C ◽  
Protein Kinase ◽  
Smooth Muscle Cells ◽  
Airway Smooth Muscle ◽  
Muscle Cells ◽  
Airway Smooth Muscle Cells ◽  
Human Airway Smooth Muscle ◽  
Human Airway ◽  
Kinase C

scholarly journals Protein Kinase C-ε Regulates Local Calcium Signaling in Airway Smooth Muscle Cells

2009 ◽  
Vol 40 (6) ◽  
pp. 663-671 ◽  
Author(s):  
Qing-Hua Liu ◽  
Yun-Min Zheng ◽  
Amit S. Korde ◽  
Xiao-Qiang Li ◽  
Jianjie Ma ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Protein Kinase C ◽  
Protein Kinase ◽  
Smooth Muscle Cells ◽  
Calcium Signaling ◽  
Airway Smooth Muscle ◽  
Muscle Cells ◽  
Airway Smooth Muscle Cells ◽  
Kinase C

Glycogen synthase kinase-3 regulates cigarette smoke extract- and IL-1β-induced cytokine secretion by airway smooth muscle

2011 ◽  
Vol 300 (6) ◽  
pp. L910-L919 ◽  
Author(s):  
Hoeke A. Baarsma ◽  
Herman Meurs ◽  
Andrew J. Halayko ◽  
Mark H. Menzen ◽  
Martina Schmidt ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Cigarette Smoke ◽  
Airway Smooth Muscle ◽  
Glycogen Synthase ◽  
Muscle Cells ◽  
Cigarette Smoke Extract ◽  
Glycogen Synthase Kinase 3 ◽  
Airway Smooth Muscle Cells ◽  
Human Airway Smooth Muscle

Glycogen synthase kinase-3 (GSK-3) is a constitutively active kinase that regulates multiple signaling proteins and transcription factors involved in inflammation. Its role in inflammatory lung diseases, including chronic obstructive pulmonary disease (COPD), is largely unknown. We investigated the role of GSK-3 in the secretion of chemokines and growth factors by human airway smooth muscle cells after exposure to cigarette smoke extract (CSE) or interleukin-1β (IL-1β), important factors involved in the development of COPD. Cultured human airway smooth muscle cells were exposed to increasing concentrations of CSE (1–15%) and IL-1β (0.01–1.0 ng/ml), which induced the secretion of VEGF-A and IL-8, whereas eotaxin secretion was induced by IL-1β only. Inhibition of GSK-3 by the selective inhibitor SB216763 or CHIR/CT99021 attenuated the cytokine and growth factor release induced by CSE and/or IL-1β, without affecting the basal release. Secretion of the cytokines by airway smooth muscle partially depends on NF-κB signaling, and GSK-3 has been implicated in regulating multiple steps in activating the NF-κB signaling pathway. IL-1β treatment induced degradation of the NF-κB inhibitory protein Iκ-Bα followed by nuclear translocation and DNA binding of p65 NF-κB, which were unaffected by inhibition of GSK-3. However, induction of NF-κB-dependent transcriptional activity by IL-1β and CSE was largely reduced upon GSK-3 inhibition by SB216763. Collectively, we demonstrate that CSE and IL-1β activate airway smooth muscle cells to secrete the proinflammatory cytokines IL-8, eotaxin, and VEGF-A. Furthermore, we show that GSK-3 regulates the release of these cytokines induced by CSE and IL-1β by promoting NF-κB-dependent gene transcription.

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