Canonical Notch signaling in the developing lung is required for determination of arterial smooth muscle cells and selection of Clara versus ciliated cell fate

Development ◽  
2010 ◽  
Vol 137 (3) ◽  
pp. e1-e1
Author(s):  
M. Morimoto ◽  
Z. Liu ◽  
H.-T. Cheng ◽  
N. Winters ◽  
D. Bader ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Notch Signaling ◽  
Cell Fate ◽  
Ciliated Cell ◽  
Muscle Cells ◽  
Arterial Smooth Muscle ◽  
Arterial Smooth Muscle Cells ◽  
Selection Of

scholarly journals Activation of Notch signaling by short-term treatment with Jagged-1 enhances store-operated Ca2+ entry in human pulmonary arterial smooth muscle cells

2014 ◽  
Vol 306 (9) ◽  
pp. C871-C878 ◽  
Author(s):  
Hisao Yamamura ◽  
Aya Yamamura ◽  
Eun A. Ko ◽  
Nicole M. Pohl ◽  
Kimberly A. Smith ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Notch Signaling ◽  
Muscle Cells ◽  
Short Term ◽  
Arterial Smooth Muscle ◽  
Pulmonary Arterial ◽  
Arterial Smooth Muscle Cells ◽  
Pulmonary Arterial Smooth Muscle ◽  
Active Fragment

Notch signaling plays a critical role in controlling proliferation and differentiation of pulmonary arterial smooth muscle cells (PASMC). Upregulated Notch ligands and Notch3 receptors in PASMC have been reported to promote the development of pulmonary vascular remodeling in patients with pulmonary arterial hypertension (PAH) and in animals with experimental pulmonary hypertension. Activation of Notch receptors by their ligands leads to the cleavage of the Notch intracellular domain (NICD) to the cytosol by γ-secretase; NICD then translocates into the nucleus to regulate gene transcription. In this study, we examined whether short-term activation of Notch functionally regulates store-operated Ca2+ entry (SOCE) in human PASMC. Treatment of PASMC with the active fragment of human Jagged-1 protein (Jag-1) for 15–60 min significantly increased the amplitude of SOCE induced by passive deletion of Ca2+ from the intracellular stores, the sarcoplasmic reticulum (SR). The Jag-1-induced enhancement of SOCE was time dependent: the amplitude was maximized at 30 min of treatment with Jag-1, which was closely correlated with the time course of Jag-1-mediated increase in NICD protein level. The scrambled peptide of Jag-1 active fragment had no effect on SOCE. Inhibition of γ-secretase by N-[ N-(3,5-difluorophenacetyl-l-alanyl)]- S-phenylglycine t-butyl ester (DAPT) significantly attenuated the Jag-1-induced augmentation of SOCE. In addition to the short-term effect, prolonged treatment of PASMC with Jag-1 for 48 h also markedly enhanced the amplitude of SOCE. These data demonstrate that short-term activation of Notch signaling enhances SOCE in PASMC; the NICD-mediated functional interaction with store-operated Ca2+ channels (SOC) may be involved in the Jag-1-mediated enhancement of SOCE in human PASMC.

scholarly journals Effects of vasopressin on ATP-sensitive and Ca2+-activated K+ channels of coronary arterial smooth muscle cells

1992 ◽  
Vol 58 ◽  
pp. 339
Author(s):  
Tetsuzo Wakatsuki ◽  
Yutaka Nakaya ◽  
Yukiko Miyoshi ◽  
Zeng Xiao-Rong ◽  
Masahiro Nomura ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Muscle Cells ◽  
Arterial Smooth Muscle ◽  
K Channels ◽  
Arterial Smooth Muscle Cells

Propagation of fast and slow intercellular Ca2+ waves in primary cultured arterial smooth muscle cells

Cell Calcium ◽  
2011 ◽  
Vol 50 (5) ◽  
pp. 459-467 ◽  
Author(s):  
Nadia Halidi ◽  
François-Xavier Boittin ◽  
Jean-Louis Bény ◽  
Jean-Jacques Meister
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Muscle Cells ◽  
Arterial Smooth Muscle ◽  
Arterial Smooth Muscle Cells
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