The development of action potential mechanism in a mouse neuronal cell line in vitro

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.

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

Journal of Biomedicine and Biotechnology ◽

10.1155/jbb/2006/69469 ◽

2006 ◽

Vol 2006 ◽

pp. 1-13 ◽

Cited By ~ 28

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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In vitro evidence of glucose-induced toxicity in GnRH secreting neurons: high glucose concentrations influence GnRH secretion, impair cell viability, and induce apoptosis in the GT1-1 neuronal cell line

Fertility and Sterility ◽

10.1016/j.fertnstert.2007.01.007 ◽

2007 ◽

Vol 88 (4) ◽

pp. 1143-1149 ◽

Cited By ~ 11

Author(s):

Lubna Pal ◽

Hsiao-Pai Chu ◽

Jun Shu ◽

Ilir Topalli ◽

Nanette Santoro ◽

...

Keyword(s):

Cell Viability ◽

Cell Line ◽

High Glucose ◽

Neuronal Cell ◽

Neuronal Cell Line ◽

Gnrh Secretion

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Glucagon Prevents Cytotoxicity Induced by Methylglyoxal in a Rat Neuronal Cell Line Model

Biomolecules ◽

10.3390/biom11020287 ◽

2021 ◽

Vol 11 (2) ◽

pp. 287

Author(s):

Mohammad Sarif Mohiuddin ◽

Tatsuhito Himeno ◽

Yuichiro Yamada ◽

Yoshiaki Morishita ◽

Masaki Kondo ◽

...

Keyword(s):

Nervous System ◽

Cell Line ◽

Neuronal Cell ◽

Cyclic Adenosine Monophosphate ◽

Diabetic Polyneuropathy ◽

Adenosine Monophosphate ◽

Protective Effects ◽

Neuroprotective Effects ◽

Neuronal Cell Line

Although diabetic polyneuropathy (DPN) is a frequent diabetic complication, no effective therapeutic approach has been established. Glucagon is a crucial hormone for glucose homeostasis but has pleiotropic effects, including neuroprotective effects in the central nervous system. However, the importance of glucagon in the peripheral nervous system (PNS) has not been clarified. Here, we hypothesized that glucagon might have a neuroprotective function in the PNS. The immortalized rat dorsal root ganglion (DRG) neuronal cell line 50B11 was treated with methylglyoxal (MG) to mimic an in vitro DPN model. The cells were cultured with or without glucagon or MG. Neurotoxicity, survival, apoptosis, neurite projection, cyclic adenosine monophosphate (cAMP), and protein kinase A (PKA) were examined. Glucagon had no cytotoxicity and rescued the cells from neurotoxicity. Cell survival was increased by glucagon. The ratio of apoptotic cells, which was increased by MG, was reduced by glucagon. Neurite outgrowth was accelerated in glucagon-treated cells. Cyclic AMP and PKA accumulated in the cells after glucagon stimulation. In conclusion, glucagon protected the DRG neuronal cells from MG-induced cellular stress. The cAMP/PKA pathway may have significant roles in those protective effects of glucagon. Glucagon may be a potential target for the treatment of DPN.

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In vitro induction of differentiation by retinoic acid in an immortalized olfactory neuronal cell line

Acta Histochemica ◽

10.1016/j.acthis.2006.10.001 ◽

2007 ◽

Vol 109 (2) ◽

pp. 111-121 ◽

Cited By ~ 3

Author(s):

Sophie Lakard ◽

Eric Lesniewska ◽

Germaine Michel ◽

Boris Lakard ◽

Nadege Morrand-Villeneuve ◽

...

Keyword(s):

Retinoic Acid ◽

Cell Line ◽

Neuronal Cell ◽

Neuronal Cell Line ◽

Induction Of Differentiation ◽

In Vitro Induction

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In vitro differentiation in a human cortical neuronal cell line (HCN-1A): Ultrastructure and immunocytochemistry

Proceedings, annual meeting, Electron Microscopy Society of America ◽

10.1017/s0424820100167937 ◽

1994 ◽

Vol 52 ◽

pp. 40-41

Author(s):

R. L. Moses ◽

J. W. Haycock

Keyword(s):

Cell Line ◽

Neuronal Cell ◽

In Situ Tem ◽

Tem Analysis ◽

Neuronal Cell Line ◽

Neuronal Markers ◽

Process Formation ◽

A Cell

The study of neuronal differentiation would be facilitated by the availability of a homogeneous neuronal cell line capable of differentiation. Ronnett, et al. have cloned a cell line (HCN-1A) from the cerebral cortex of a megalencephalic patient. These cells undergo process formation after treatment with nerve growth factor and cAMP and, after differentiation, express numerous neuronal markers. Subsequent to treatment, the normally epithelioid HCN-1A cells became highly branched, often within the first two hours (FIG. 1A), creating a meshwork of closely associated processes with several orders of branching (FIG 1B). Not all cells remained in the differentiated state, resulting in phenotypically mixed cultures (FIG. 1A). Light microscopy of treated cells suggested that process formation occurred via cytoplasmic retraction rather than neurite outgrowth. In situ TEM analysis revealed that the cell bodies (FIG. 2A) of treated and untreated cells both possessed a number of neuronal characteristics including large euchromatic nuclei with prominent nucleoli, numerous profiles of rough endoplasmic reticulum (FIG. 2B), and prominent Golgi lamellae (FIG. 2C). Processes (FIG. 2D) were not ultrastructurally identifiable as axonal versus dendritic. Longitudinally arranged microtubules and intermediate filaments were both present in the majority of processes.

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Nitric oxide inhibits the expression of AT1 receptors in neurons

AJP Cell Physiology ◽

10.1152/ajpcell.00258.2011 ◽

2012 ◽

Vol 302 (8) ◽

pp. C1162-C1173 ◽

Cited By ~ 20

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.

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