scholarly journals DNA-dependent protein kinase (DNA-PK) permits vascular smooth muscle cell proliferation through phosphorylation of the orphan nuclear receptor NOR1

2015 ◽  
Vol 106 (3) ◽  
pp. 488-497 ◽  
Author(s):  
S. Medunjanin ◽  
J.-M. Daniel ◽  
S. Weinert ◽  
J. Dutzmann ◽  
F. Burgbacher ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Smooth Muscle ◽  
Protein Kinase ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cell ◽  
Nuclear Receptor ◽  
Muscle Cell ◽  
Orphan Nuclear Receptor ◽  
Dependent Protein Kinase ◽  
Dependent Protein

scholarly journals The NR4A Orphan Nuclear Receptor NOR1 Is Induced by Platelet-derived Growth Factor and Mediates Vascular Smooth Muscle Cell Proliferation

2006 ◽  
Vol 281 (44) ◽  
pp. 33467-33476 ◽  
Author(s):  
Takashi Nomiyama ◽  
Takafumi Nakamachi ◽  
Florence Gizard ◽  
Elizabeth B. Heywood ◽  
Karrie L. Jones ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Smooth Muscle ◽  
Growth Factor ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cell ◽  
Nuclear Receptor ◽  
Muscle Cell ◽  
Vascular Smooth Muscle Cell ◽  
Platelet Derived Growth Factor ◽  
Orphan Nuclear Receptor

Modulation of pulmonary vascular smooth muscle cell phenotype in hypoxia: role of cGMP-dependent protein kinase

2007 ◽  
Vol 292 (6) ◽  
pp. L1459-L1466 ◽  
Author(s):  
Weilin Zhou ◽  
Chiranjib Dasgupta ◽  
Sewite Negash ◽  
J. Usha Raj
Keyword(s):  
Smooth Muscle ◽  
Protein Kinase ◽  
Vascular Smooth Muscle ◽  
Protein Expression ◽  
Smooth Muscle Cell ◽  
Muscle Cell ◽  
Dependent Protein Kinase ◽  
Cgmp Dependent Protein Kinase ◽  
Marker Proteins ◽  
Dependent Protein

Chronic hypoxia triggers pulmonary vascular remodeling, which is associated with a modulation of the vascular smooth muscle cell (SMC) phenotype from a contractile, differentiated to a synthetic, dedifferentiated state. We previously reported that acute hypoxia represses cGMP-dependent protein kinase (PKG) expression in ovine fetal pulmonary venous SMCs (FPVSMCs). Therefore, we tested if altered expression of PKG could explain SMC phenotype modulation after exposure to hypoxia. Hypoxia-induced reduction in PKG protein expression strongly correlated with the repressed expression of SMC phenotype markers, myosin heavy chain (MHC), calponin, vimentin, α-smooth muscle actin (αSMA), and thrombospondin (TSP), indicating that hypoxic exposure of SMC induced phenotype modulation to dedifferentiated state, and PKG may be involved in SMC phenotype modulation. PKG-specific small interfering RNA (siRNA) transfection in FPVSMCs significantly attenuated calponin, vimentin, and MHC expression, with no effect on αSMA and TSP. Treatment with 30 μM Drosophila Antennapedia (DT-3), a membrane-permeable peptide inhibitor of PKG, attenuated the expression of TSP, MHC, αSMA, vimentin, and calponin. The results from PKG siRNA and DT-3 studies indicate that hypoxia-induced reduction in protein expression was also similarly impacted by PKG inhibition. Overexpression of PKG in FPVSMCs by transfection with a full-length PKG construct tagged with green fluorescent fusion protein (PKG-GFP) reversed the effect of hypoxia on the expression of SMC phenotype marker proteins. These results suggest that PKG could be one of the determinants for the expression of SMC phenotype marker proteins and may be involved in the maintenance of the differentiated phenotype in pulmonary vascular SMCs in hypoxia.

Cyclic GMP-Dependent Protein Kinase Regulates Vascular Smooth Muscle Cell Phenotype

1997 ◽  
Vol 34 (4) ◽  
pp. 245-259 ◽  
Author(s):  
Nancy J. Boerth ◽  
Nupur B. Dey ◽  
Trudy L. Comwell ◽  
Thomas M. Lincoln
Keyword(s):  
Smooth Muscle ◽  
Protein Kinase ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cell ◽  
Muscle Cell ◽  
Cyclic Gmp ◽  
Cell Phenotype ◽  
Dependent Protein Kinase ◽  
Smooth Muscle Cell Phenotype ◽  
Dependent Protein
Sign in / Sign up

Export Citation Format

Share Document