scholarly journals Acetyl-L-Carnitine Modulates TP53 and IL10 Gene Expression Induced by 3-NPA Evoked Toxicity in PC12 Cells

2011 ◽  
Vol 9 (1) ◽  
pp. 195-199 ◽  
Author(s):  
A. Virmani ◽  
A. Koverech ◽  
S. F. Ali ◽  
Z. K. Binienda
Keyword(s):  
Gene Expression ◽  
Pc12 Cells ◽  
Il10 Gene

scholarly journals Elevation of gene expression of Btg2, Gadd 153, and antioxidant markers in RONS-induced PC12 cells

2020 ◽  
Vol 9 (1) ◽  
Author(s):  
Aravind P ◽  
Sarojini R. Bulbule ◽  
Hemalatha N ◽  
Anushree G ◽  
Babu R.L ◽  
...  
Keyword(s):  
Gene Expression ◽  
Endoplasmic Reticulum ◽  
Protein Expression ◽  
Pc12 Cells ◽  
Expression Pattern ◽  
High Glucose ◽  
Nitrosative Stress ◽  
Gene Expression Pattern ◽  
Marker Genes ◽  
Differential Stress

Abstract Background Free radicals generated in the biological system bring about modifications in biological molecules causing damage to their structure and function. Identifying the damage caused by ROS and RNS is important to predict the pathway of apoptosis due to stress in PC12 cells. The first defense mechanisms against them are antioxidants which act in various pathways through important cellular organelles like the mitochondria and endoplasmic reticulum. Specific biomarkers like Gadd153 which is a marker for endoplasmic reticulum stress, Nrf2 which responds to the redox changes and translocates the antioxidant response elements, and Btg2 which is an antioxidant regulator have not been addressed in different stress conditions previously in PC12 cells. Therefore, the study was conducted to analyze the gene expression pattern (SOD, Catalase, Btg2, Gadd153, and Nrf2) and the protein expression pattern (iNOS and MnSOD) of the antioxidant stress markers in differential stress-induced PC12 cells. Peroxynitrite (1 μM), rotenone (1 μM), H2O2(100 mM), and high glucose (33 mM) were used to induce oxidative and nitrosative stress in PC12 cells. Results The results obtained suggested that rotenone-induced PC12 cells showed a significant increase in the expression of catalase, Btg2, and Gadd153 compared to the control. Peroxynitrite-induced PC12 cells showed higher expression of Btg2 compared to the control. H2O2 and high glucose showed lesser expression compared to the control in all stress marker genes. In contrast, the Nrf2 gene expression is downregulated in all the stress-induced PC12 cells compared to the control. Further, MnSOD and iNOS protein expression studies suggest that PC12 cells exhibit a selective downregulation. Lower protein expression of MnSOD and iNOS may be resulted due to the mitochondrial dysfunction in peroxynitrite-, high glucose-, and H2O2-treated cells, whereas rotenone-induced cells showed lower expression, which could be the result of a dysfunction of the endoplasmic reticulum. Conclusion Different stress inducers like rotenone, peroxynitrite, H2O2, and high glucose increase the NO and ROS. Btg2 and Gadd153 genes were upregulated in the stress-induced cells, whereas the Nrf2 was significantly downregulated in differential stress-induced PC12 cells. Further, antioxidant marker genes were differentially expressed with different stress inducers.

scholarly journals Neurosecretion competence. A comprehensive gene expression program identified in PC12 cells.

2002 ◽  
Vol 277 (48) ◽  
pp. 46840
Author(s):  
Christophe Grundschober ◽  
Maria Luisa Malosio ◽  
Laura Astolfi ◽  
Tiziana Giordano ◽  
Patrick Nef ◽  
...  
Keyword(s):  
Gene Expression ◽  
Pc12 Cells ◽  
Gene Expression Program ◽  
Expression Program

Gene expression profiling in PC12 cells infected with an oncolytic Newcastle disease virus strain

2014 ◽  
Vol 185 ◽  
pp. 10-22 ◽  
Author(s):  
András Balogh ◽  
Judit Bátor ◽  
Lajos Markó ◽  
Mária Németh ◽  
Marianna Pap ◽  
...  
Keyword(s):  
Gene Expression ◽  
Newcastle Disease Virus ◽  
Gene Expression Profiling ◽  
Pc12 Cells ◽  
Disease Virus ◽  
Virus Strain ◽  
Newcastle Disease ◽  
Expression Profiling ◽  
Newcastle Disease Virus Strain

scholarly journals Contrasting Roles of Ang II and ACEA in the Regulation of IL10 and IL1β Gene Expression in Primary SHR Astroglial Cultures

Molecules ◽  
2021 ◽  
Vol 26 (10) ◽  
pp. 3012
Author(s):  
Dhanush Haspula ◽  
Michelle A. Clark
Keyword(s):  
Gene Expression ◽  
Wistar Rats ◽  
Gene Signature ◽  
Brain Regions ◽  
Inhibitory Effect ◽  
Ang Ii ◽  
Cannabinoid Type 1 Receptor ◽  
Il10 Gene ◽  
Cerebellar Astrocytes

Angiotensin (Ang) II is well-known to have potent pro-oxidant and pro-inflammatory effects in the brain. Extensive crosstalk between the primary Ang II receptor, Ang type 1 receptor (AT1R), and the cannabinoid type 1 receptor (CB1R) has been demonstrated by various groups in the last decade. Since activation of glial CB1R has been demonstrated to play a key role in the resolution of inflammatory states, we investigated the role of Ang II (100 nM) and/or ACEA (10 nM), a potent CB1R-specific agonist in the regulation of inflammatory markers in astrocytes from spontaneously hypertensive rats (SHR) and Wistar rats. Astrocytes were cultured from brainstems and cerebellums of SHR and Wistar rats and assayed for IL1β and IL10 gene expression and secreted fraction, in treated and non-treated cells, by employing qPCR and ELISA, respectively. mRNA expression of both IL10 and IL1β were significantly elevated in untreated brainstem and cerebellar astrocytes isolated from SHR when compared to Wistar astrocytes. No changes were observed in the secreted fraction. While ACEA-treatment resulted in a significant increase in IL10 gene expression in Wistar brainstem astrocytes (Log2FC ≥ 1, p < 0.05), its effect in SHR brainstem astrocytes was diminished. Ang II treatment resulted in a strong inhibitory effect on IL10 gene expression in astrocytes from both brain regions of SHR and Wistar rats (Log2FC ≤ −1, p < 0.05), and an increase in IL1β gene expression in brainstem astrocytes from both strains (Log2FC ≥ 1, p < 0.05). Co-treatment of Ang II and ACEA resulted in neutralization of Ang II-mediated effect in Wistar brainstem and cerebellar astrocytes, but not SHR astrocytes. Neither Ang II nor ACEA resulted in any significant changes in IL10 or IL1β secreted proteins. These data suggest that Ang II and ACEA have opposing roles in the regulation of inflammatory gene signature in astrocytes isolated from SHR and Wistar rats. This however does not translate into changes in their secreted fractions.

Effect of a dominant inhibitory Ha-ras mutation on neuronal differentiation of PC12 cells

1990 ◽  
Vol 10 (10) ◽  
pp. 5324-5332
Author(s):  
J Szeberényi ◽  
H Cai ◽  
G M Cooper
Keyword(s):  
Gene Expression ◽  
Growth Factor ◽  
Neuronal Differentiation ◽  
Pc12 Cells ◽  
Morphological Differentiation ◽  
Early Response ◽  
Secondary Response ◽  
Response Gene ◽  
Early Response Gene ◽  
Early Response Genes

A dominant inhibitory mutation of Ha-ras which changes Ser-17 to Asn-17 in the gene product p21 [p21 (Asn-17)Ha-ras] has been used to investigate the role of ras in neuronal differentiation of PC12 cells. The growth of PC12 cells, in contrast to NIH 3T3 cells, was not inhibited by p21(Asn-17)Ha-ras expression. However, PC12 cells expressing the mutant Ha-ras protein showed a marked inhibition of morphological differentiation induced by nerve growth factor (NGF) or fibroblast growth factor (FGF). These cells, however, were still able to respond with neurite outgrowth to dibutyryl cyclic AMP and 12-O-tetradecanoylphorbol-13-acetate (TPA). Induction of early-response genes (fos, jun, and zif268) by NGF and FGF but not by TPA was also inhibited by high levels of p21(Asn-17)Ha-ras. However, lower levels of p21(Asn-17) expression were sufficient to block neuronal differentiation without inhibiting induction of these early-response genes. Induction of the secondary-response genes SCG10 and transin by NGF, like morphological differentiation, was inhibited by low levels of p21(Asn-17) whether or not induction of early-response genes was blocked. Therefore, although inhibition of ras function can inhibit early-response gene induction, this is not required to block morphological differentiation or secondary-response gene expression. These results suggest that ras proteins are involved in at least two different pathways of signal transduction from the NGF receptor, which can be distinguished by differential sensitivity to p21(Asn-17)Ha-ras. In addition, ras and protein kinase C can apparently induce early-response gene expression by independent pathways in PC12 cells.

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