scholarly journals Nitric oxide inhibits the expression of AT1 receptors in neurons

2012 ◽  
Vol 302 (8) ◽  
pp. C1162-C1173 ◽  
Author(s):  
Neeru M. Sharma ◽  
Hong Zheng ◽  
Yi-Fan Li ◽  
Kaushik P. Patel
Keyword(s):  
Nitric Oxide ◽  
Cell Line ◽  
Control Level ◽  
Neuronal Cell ◽  
Ang Ii ◽  
No Donor ◽  
Neuronal Cell Line ◽  
Adenoviral Gene Transfer ◽  
Dose Dependent

We have previously observed an increased of angiotensin II (ANG II) type 1 receptor (AT1R) with enhanced AT1R-mediated sympathetic outflow and concomitant downregulation of neuronal nitric oxide (NO) synthase (nNOS) with reduced NO-mediated inhibition from the paraventricular nucleus (PVN) in rats with heart failure. To test the hypothesis that NO exerts an inhibitory effect on AT1R expression in the PVN, we used primary cultured hypothalamic cells of neonatal rats and neuronal cell line NG108-15 as in vitro models. In hypothalamic primary culture, NO donor sodium nitroprusside (SNP) induced dose-dependent decreases in mRNA and protein of AT1R (10−5 M SNP, AT1R protein was 10 ± 2% of control level) while NOS inhibitor NG-monomethyl-l-arginine (l-NMMA) induced dose-dependent increases in mRNA and protein levels of AT1R (10−5 M l-NMMA, AT1R protein was 148 ± 8% of control level). Similar effects of SNP and l-NMMA on AT1R expression were also observed in NG108-15 cell line (10−6 M SNP, AT1R protein was 30 ± 4% of control level while at the dose of 10−6 M l-NMMA, AT1R protein was 171 ± 15% of the control level). Specific inhibition of nNOS, using antisense, caused an increase in AT1R expression while overexpression of nNOS, using adenoviral gene transfer (Ad.nNOS), caused an inhibition of AT1R expression in NG108 cells. Antisense nNOS transfection augmented the increase while Ad.nNOS infection blunted the increase in intracellular calcium concentration in response to ANG II treatment in NG108 cells. In addition, downregulation of AT1R mRNA as well as protein level in neuronal cell line in response to S-nitroso- N-acetyl pencillamine (SNAP) treatment was blocked by protein kinase G (PKG) inhibitor, while the peroxynitrite scavenger deforxamine had no effect. These results suggest that NO acts as an inhibitory regulator of AT1R expression and the activation of PKG is the required step in the regulation of AT1R gene expression via cGMP-dependent signaling pathway.

scholarly journals In Vitro Induction of Apoptosis or Differentiation by Dopamine in an Immortalized Olfactory Neuronal Cell Line

2002 ◽  
Vol 69 (5) ◽  
pp. 1870-1881 ◽  
Author(s):  
V. Coronas ◽  
F. Féron ◽  
R. Hen ◽  
G. Sicard ◽  
F. Jourdan ◽  
...  
Keyword(s):  
Cell Line ◽  
Neuronal Cell ◽  
Neuronal Cell Line ◽  
Induction Of Apoptosis ◽  
In Vitro Induction

Effects of Estrogen and Phytoestrogen Treatment on an In Vitro Model of Recurrent Stroke on HT22 Neuronal Cell Line

2016 ◽  
Vol 37 (3) ◽  
pp. 405-416 ◽  
Author(s):  
Javier Morán ◽  
Marcos Perez-Basterrechea ◽  
Pablo Garrido ◽  
Elena Díaz ◽  
Ana Alonso ◽  
...  
Keyword(s):  
Cell Line ◽  
In Vitro Model ◽  
Recurrent Stroke ◽  
Neuronal Cell ◽  
Neuronal Cell Line ◽  
Vitro Model

scholarly journals New ways to print living cells promise breakthroughs for engineering complex tissues in vitro

2006 ◽  
Vol 394 (2) ◽  
Author(s):  
Ginger S. Withers
Keyword(s):  
Tissue Engineering ◽  
Cell Growth ◽  
Cell Line ◽  
Neuronal Cell ◽  
Living Cells ◽  
Neuronal Cell Line ◽  
Biochemical Journal ◽  
Electrohydrodynamic Printing ◽  
Cell Networks

The ability to control the placement of cells and the assembly of networks in vitro has tremendous potential for understanding the regulation of development as well as for generating artificial tissues. To date, most engineering tools that can place materials with precision are not compatible with the requirements of living cells, and so approaches to tissue engineering have focused on patterning substrates as a way of controlling cell growth rather than patterning cells directly. In this issue of Biochemical Journal, however, Eagles et al. adapt electrohydrodynamic printing technology to ‘print’ living cells from a neuronal cell line on to a substrate. The importance of this approach is that it has the potential for unprecedented control over the position of cells in culture by directly placing them, thus allowing for the systematic assembly of cell networks.

scholarly journals Cellular Prion Protein and Caveolin-1 Interaction in a Neuronal Cell Line Precedes Fyn/Erk 1/2 Signal Transduction

2006 ◽  
Vol 2006 ◽  
pp. 1-13 ◽  
Author(s):  
Mattia Toni ◽  
Enzo Spisni ◽  
Cristiana Griffoni ◽  
Spartaco Santi ◽  
Massimo Riccio ◽  
...  
Keyword(s):  
Signal Transduction ◽  
Cell Line ◽  
Prion Protein ◽  
Neuronal Cell ◽  
Cellular Prion Protein ◽  
Glutathione S Transferase ◽  
Neuronal Cell Line ◽  
Caveolin 1 ◽  
Fyn Kinase

It has been reported that cellular prion protein (PrPc) is enriched in caveolae or caveolae-like domains with caveolin-1 (Cav-1) participating to signal transduction events by Fyn kinase recruitment. By using the Glutathione-S-transferase (GST)-fusion proteins assay, we observed that PrPc strongly interacts in vitro with Cav-1. Thus, we ascertained the PrPc caveolar localization in a hypothalamic neuronal cell line (GN11), by confocal microscopy analysis, flotation on density gradient, and coimmunoprecipitation experiments. Following the anti-PrPc antibody-mediated stimulation of live GN11 cells, we observed that PrPc clustered on plasma membrane domains rich in Cav-1 in which Fyn kinase converged to be activated. After these events, a signaling cascade through p42/44 MAP kinase (Erk 1/2) was triggered, suggesting that following translocations from rafts to caveolae or caveolae-like domains PrPc could interact with Cav-1 and induce signal transduction events.

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