Phosphatidylinositol 3-kinase in angiotensin II-induced hypertrophy of vascular smooth muscle cells

2003 ◽  
Vol 478 (1) ◽  
pp. 39-46 ◽  
Author(s):  
Tadashi Yamakawa ◽  
Shun-ichi Tanaka ◽  
Junzo Kamei ◽  
Kazuaki Kadonosono ◽  
Kenji Okuda
Keyword(s):  
Smooth Muscle ◽  
Angiotensin Ii ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Muscle Cells ◽  
Phosphatidylinositol 3 Kinase ◽  
Phosphatidylinositol 3

Rapamycin antagonizes NF-κB nuclear translocation activated by TNF-α in primary vascular smooth muscle cells and enhances apoptosis

2006 ◽  
Vol 290 (6) ◽  
pp. H2459-H2465 ◽  
Author(s):  
Arturo Giordano ◽  
Raffaella Avellino ◽  
Paolo Ferraro ◽  
Simona Romano ◽  
Nicola Corcione ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Nuclear Translocation ◽  
Muscle Cells ◽  
Phosphatidylinositol 3 Kinase ◽  
Tnf Α ◽  
Iκbα Degradation ◽  
Phosphatidylinositol 3

Several lines of evidence support the view that rapamycin inhibits NF-κB. TNF-α, a potent inducer of NF-κB, is released after artery injury (e.g., balloon angioplasty) and plays an important role in inflammation and restenosis. We investigated the effect of rapamycin on NF-κB activation and apoptosis in vascular smooth muscle cells (VSMCs) stimulated with TNF-α. Using EMSA, we found that TNF-α caused NF-κB nuclear translocation in VSMCs after 1 h of incubation. Rapamycin inhibited IκBα degradation, thereby preventing nuclear translocation. Activation of NF-κB was accompanied by an increase of Bcl-xL and Bfl-1/A1 proteins, detected by Western blot assay, whereas rapamycin prevented the TNF-α-induced enhancement of these antiapoptotic proteins. The extent of apoptosis of VSMCs exposed to TNF-α was significantly enhanced by rapamycin. The effect of rapamycin appeared to be independent of the phosphatidylinositol 3-kinase/Akt-protein kinase B survival pathway, because the phosphatidylinositol 3-kinase inhibitor wortmannin neither prevented IκBα degradation nor increased apoptosis of cells incubated with TNF-α. Finally, we demonstrate that the large immunophilin FK-506 binding protein FKBP51 is essential for TNF-α-induced NF-κB activation in VSMCs. Our findings show that rapamycin inhibits NF-κB activation and acts in concert with TNF-α in induction of VSMC apoptosis.

scholarly journals Axl/Phosphatidylinositol 3-Kinase Signaling Inhibits Mineral Deposition by Vascular Smooth Muscle Cells

2007 ◽  
Vol 100 (4) ◽  
pp. 502-509 ◽  
Author(s):  
Georgina D.M. Collett ◽  
Andrew P. Sage ◽  
John Paul Kirton ◽  
M. Yvonne Alexander ◽  
Andrew P. Gilmore ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Muscle Cells ◽  
Kinase Signaling ◽  
Phosphatidylinositol 3 Kinase ◽  
Mineral Deposition ◽  
Phosphatidylinositol 3
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