Wyniki wyszukiwania

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The modulatory effect of flavonoid glycosides on angiotensin II stimulated PC 12 cells

100%

Zielinski B., Berdowska I., Seweryn E., Ceremuga I., Chwilkowska A., Fecka I., Banas T.

Cellular and Molecular Biology Letters

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2002

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tom 07

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nr Suppl.

2

Protective effects of nicotine against glutamate-induced neurotoxicity in PC12 cells

88%

Sun X., Liu Y., Hu G., Wang H.

Cellular and Molecular Biology Letters

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2004

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tom 09

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nr 3

This study aimed to assess whether nicotine prevented glutamate neurotoxicity in PC12 cells, and to identify the molecular mechanisms of any effects. The results showed that glutamate neurotoxicity in PC12 cells could be prevented by treatment with nicotine at concentrations of 10 nmol.l-1-1 mmol.l-1. This effect was in turn found to be inhibited by the application of the nicotinic acetylcholine receptor (nAChR) antagonist mecamylamine. Nicotine significantly decreased the basal level of intracellular free Ca2+ and enhanced the buffering action on Ca2+ overload induced by high concentrations of glutamate (5 mmol.l-1). In addition, nicotine treatment up-regulated the mRNA and protein expression of apoptosis-related factors including bcl-2 mRNA and protein, but down-regulated the expression of bax mRNA and protein. It is concluded that the protective effects of nicotine against the neurotoxicity induced by glutamate are mediated by nAChRs, due to the increased buffering action on Ca2+ and the modulation of apoptotic processes.

3

The effect of antisense oligonucleotide treatment of plasma membrane Ca2plus-ATPase in PC12 cells

75%

Szemraj J., Kawecka I., Bartkowiak J., Zylinska L.

Cellular and Molecular Biology Letters

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2004

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tom 09

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nr 3

Plasma membrane Ca2+-ATPase (PMCA), encoded by four separate genes, constitutes a high affinity system extruding Ca2+ outside the cell. The nerve growth factor-treated PC12 cell line possesses all four main PMCA isoforms. To evaluate the potential role of PMCA isoforms in the differentiation process, we transiently suppressed the expression of PMCA2 and 3 using the antisense oligonucleotides. In the transfected PC12 cells, we observed morphological changes, slowed neurite extension and diminished survival of the cells. The apparent transport activity and affinity of the calcium pump to Ca2+ were lower in the cells with suppressed PMCA2 and 3 isoforms than in the control cells. Moreover, in the transfected PC12 plasma membranes, the calcium pump was insensitive to stimulation by calmodulin. These findings suggest that PMCA2 and 3 isoforms may be involved in developmental and differentiation processes.

4

Direct Rho-associated kinase inhibition induces cofilin dephosphorylation and neurite outgrowth in PC-12 cells

75%

Zhang Z., Ottens A. K., Larner S. F., Kobeissy F. H., Williams M. L., Hayes R. L., Wang K. K. W.

Cellular and Molecular Biology Letters

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2006

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tom 11

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nr 1

Axons fail to regenerate in the adult central nervous system (CNS) following injury. Developing strategies to promote axonal regeneration is therapeutically attractive for various CNS pathologies such as traumatic brain injury, stroke and Alzheimer’s disease. Because the RhoA pathway is involved in neurite outgrowth, Rho-associated kinases (ROCKs), downstream effectors of GTP-bound Rho, are potentially important targets for axonal repair strategies in CNS injuries. We investigated the effects and downstream mechanisms of ROCK inhibition in promoting neurite outgrowth in a PC-12 cell model. Robust neurite outgrowth (NOG) was induced by ROCK inhibitors Y-27632 and H-1152 in a time-and dose-dependent manner. Dramatic cytoskeletal reorganization was noticed upon ROCK inhibition. NOG initiated within 5 to 30 minutes followed by neurite extension between 6 and 10 hours. Neurite processes were then sustained for over 24 hours. Rapid cofilin dephosphorylation was observed within 5 minutes of Y-27632 and H-1152 treatment. Re-phosphorylation was observed by 6 hours after Y-27632 treatment, while H-1152 treatment produced sustained cofilin dephosphorylation for over 24 hours. The results suggest that ROCK-mediated dephosphorylation of cofilin plays a role in the initiation of NOG in PC-12 cells.

5

Myosin VI is associated with secretory granules and is present in the nucleus in adrenal medulla chromaffin cells

63%

Majewski L., Sobczak M., Redowicz M. J.

Acta Biochimica Polonica

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2010

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tom 57

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nr 1

109-114

Myosin VI (MVI) is the only known myosin walking towards minus end of actin filaments. Here, MVI, but not myosins IB or IIB, was detected in chromaffin granules isolated from bovine medulla and found to be tightly associated with the granule apical surface. MVI also localized to secretory granules within rat pheochromocytoma PC12 cells as well as to the Golgi apparatus, endoplasmic reticulum and clathrin-coated pits. Notably, it was also found in the nucleus. RT-PCR revealed that MVI splice variants with a large insert (LI), characteristic of polarized cells, were barely detectable in PC12 cells, whereas variants with a small insert (SI) were the major isoforms. The presented data indicate that MVI in adrenal medulla cells is engaged in secretory vesicle trafficking within the cytoplasm and possibly also involved in transport within the nucleus.

6

Molecular mechanism of PC12 cell death evoked by sodium nitroprusside, a nitric oxide donor

63%

Pytlowany M., Strosznajder J. B., Jesko H., Cakala M., Strosznajder R. P.

Acta Biochimica Polonica

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2008

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tom 55

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nr 2

339-347

Nitric oxide (NO) is a potent extracellular and intracellular physiological messenger. However, NO liberated in excessive amounts can be involved in macromolecular and mitochondrial damage in brain aging and in neurodegenerative disorders. The molecular mechanism of its neurotoxic action is not fully understood. Our previous data indicated involvement of NO in the release of arachidonic acid (AA), a substrate for cyclo- and lipoxygenases (COX and LOX, respectively). In this study we investigated biochemical processes leading to cell death evoked by an NO donor, sodium nitroprusside (SNP). We found that SNP decreased viability of pheochromocytoma (PC12) cells in a concentration- and time-dependent manner. SNP at 0.1 mM caused a significant increase of apoptosis-inducing factor (AIF) protein level in mitochondria. Under these conditions 80% of PC12 cells survived. The enhancement of mitochondrial AIF level might protect most of PC12 cells against death. However, NO released from 0.5 mM SNP induced massive cell death but had no effect on protein level and localization of AIF and cytochrome c. Caspase-3 activity and poly(ADP-ribose) polymerase-1 (PARP-1) protein levels were not changed. However, PARP activity significantly decreased in a time-dependent manner. Inhibition of both COX isoforms and of 12/15-LOX significantly lowered the SNP-evoked cell death. We conclude that AIF, cytochrome cand caspase-3 are not responsible for the NO-mediated cell death evoked by SNP. The data demonstrate that NO liberated in excess decreases PARP-1 activity. Our results indicate that COX(s) and LOX(s) are involved in PC12 cell death evoked by NO released from its donor, SNP.

7

Thiamine deficiency caused by thiamine antagonists triggers upregulation of apoptosis inducing factor gene expression and leads to caspase 3-mediated apoptosis is neuronally differentiated rat PC-12 cells

63%

Chornyy S., Parkhomenko J., Chorna N.

Acta Biochimica Polonica

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2007

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tom 54

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nr 2

Recent evidence suggests that alterations in oxidative metabolism induced by thiamine deficiency lead to neuronal cell death. However, the molecular mechanisms underlying this process are still under extensive investigation. Here, we report that rat pheochromocytoma PC-12 cells differentiated in the presence of NGF into neurons undergo apoptosis due to thiamine deficiency caused by antagonists of thiamine - amprolium, pyrithiamine and oxythiamine. Confocal laser scanning fluorescence microscopy revealed that annexin V binds to PC-12 cells in presence of thiamine antagonists after 72 h incubation. Results also show that thiamine antagonists trigger upregulation of gene expression of mitochondrial-derived apoptosis inducing factor, DNA fragmentation, cleavage of caspase 3 and translocation of active product to the nucleus. We therefore propose that apoptosis induced by amprolium, pyrithiamine or oxythiamine occurs via the mitochondria-dependent caspase 3-mediated signaling pathway. In addition, our data indicate that pyrithiamine and oxythiamine are more potent inducers of apoptosis than amprolium.

8

Sodium nitroprusside, a nitric oxide donor, fails to bypass the block of neuronal differentiation in PC12 cells imposed by a dominant negative Ras protein

51%

Bator J., Varga J., Berta G., Barbakadze T., Mikeladze D., Ramsden J., Szeberenyi J.

Cellular and Molecular Biology Letters

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2012

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tom 17

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nr 3

Nitric oxide (NO) is a mediator of a diverse array of inter- and intracellular signal transduction processes. The aim of the present study was to analyze its possible role as a second messenger in the process of neuronal differentiation of PC12 pheochromocytoma cells. Upon NGF treatment wildtype PC12 cells stop dividing and develop neurites. In contrast, a PC12 subclone (designated M-M17-26) expressing a dominant-negative mutant Ras protein keeps proliferating and fails to grow neurites after NGF treatment. Sodium nitroprusside (SNP), an NO donor, was found to induce the p53 protein and to inhibit proliferation of both PC12 and M-M17-26 cells, but failed to induce neuronal differentiation in these cell lines. Key signaling pathways (the ERK and Akt pathways) were also not affected by SNP treatment, and the phosphorylation of CREB transcription factor was only slightly stimulated. It is thus concluded from the results presented in this paper that NO is unable to activate signaling proteins acting downstream or independent of Ras that are required for neuronal differentiation.

9

Extracellular signal-regulated kinases, p38 and c-Jun N-terminal kinases phosphorylation changes in PC12 cells with diabetic disturbances and comorbid excitotoxicity - a preliminary report

51%

Rorbach-Dolata A., Piwowar A.

Journal of Physiology and Pharmacology

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2020

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tom 71

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nr 5

Ograniczanie wyników

The modulatory effect of flavonoid glycosides on angiotensin II stimulated PC 12 cells

Protective effects of nicotine against glutamate-induced neurotoxicity in PC12 cells

The effect of antisense oligonucleotide treatment of plasma membrane Ca2plus-ATPase in PC12 cells

Direct Rho-associated kinase inhibition induces cofilin dephosphorylation and neurite outgrowth in PC-12 cells

Myosin VI is associated with secretory granules and is present in the nucleus in adrenal medulla chromaffin cells

Molecular mechanism of PC12 cell death evoked by sodium nitroprusside, a nitric oxide donor

Thiamine deficiency caused by thiamine antagonists triggers upregulation of apoptosis inducing factor gene expression and leads to caspase 3-mediated apoptosis is neuronally differentiated rat PC-12 cells

Sodium nitroprusside, a nitric oxide donor, fails to bypass the block of neuronal differentiation in PC12 cells imposed by a dominant negative Ras protein

Extracellular signal-regulated kinases, p38 and c-Jun N-terminal kinases phosphorylation changes in PC12 cells with diabetic disturbances and comorbid excitotoxicity - a preliminary report