scholarly journals Effect of Rho-associated kinase inhibition on actin cytoskeleton structure and calcium response in glioma C6 cells.

2006 ◽  
Vol 53 (4) ◽  
pp. 825-831 ◽  
Author(s):  
Berenika Targos ◽  
Paweł Pomorski ◽  
Patryk Krzemiński ◽  
Jolanta Barańska ◽  
Maria Jolanta Redowicz ◽  
...  
Keyword(s):  
Actin Cytoskeleton ◽  
Calcium Signaling ◽  
Functional State ◽  
Myosin Ii ◽  
Calcium Signal ◽  
Second Phase ◽  
C6 Cells ◽  
Calcium Response ◽  
Glioma C6 ◽  
Cytoskeleton Reorganization

The role of actin cytoskeleton functional state in glioma C6 cell morphology and calcium signaling was investigated through modification of myosin II activity by blocking Rho-associated kinase with the specific inhibitor Y-27632. Treatment of glioma C6 cells with ROCK inhibitor resulted in actin cytoskeleton reorganization and also in the changed shape and distribution of mitochondria. Changes in the distribution of ER, the main calcium store in glioma C6 cells, were not visible. The inhibition of myosin II activity influences the first phase of calcium signaling evoked by agonist, and both phases of thapsigargin-evoked calcium response. We suggest that the observed increase in Ca2+ release from intracellular stores induced by IP3 formation as well as inhibition of SERCA ATPase is at least in part related to severely affected mitochondria. Enhancement of capacitative calcium entry evoked by thapsigargin is probably associated with the reorganization of the acto-myosin II system. ATP-induced calcium response presents no changes in the second phase. We observed that ATP stimulation of Y-27632 pretreated cells leads to immediate morphological rearrangement of glioma C6 cells. It is a consequence of actin cytoskeleton reorganization: formation of stress fibers and relocation of phosphorylated myosin II to actin filaments. It seems that the agonist-evoked strong calcium signal may be sufficient for myosin II activation and the stress fiber organization. This is the first work showing the dependence between the functional state of the acto-myosin II system and calcium signaling stressing the reversible character of this relationship.

scholarly journals Is MLC phosphorylation essential for the recovery from ROCK inhibition in glioma C6 cells?

2011 ◽  
Vol 58 (1) ◽  
Author(s):  
Jarosław Korczyński ◽  
Katarzyna Sobierajska ◽  
Patryk Krzemiński ◽  
Anna Wasik ◽  
Dorota Wypych ◽  
...  
Keyword(s):  
Actin Cytoskeleton ◽  
Cell Morphology ◽  
C6 Cells ◽  
Cytoskeleton Organization ◽  
Glioma C6 ◽  
Cytoskeleton Reorganization ◽  
Actin Cytoskeleton Organization ◽  
Rock Inhibition ◽  
Cytoskeleton Dynamics ◽  
Mlc Phosphorylation

Inhibition of Rho-associated protein kinase (ROCK) activity in glioma C6 cells induces changes in actin cytoskeleton organization and cell morphology similar to those observed in other types of cells with inhibited RhoA/ROCK signaling pathway. We show that phosphorylation of myosin light chains (MLC) induced by P2Y₂ receptor stimulation in cells with blocked ROCK correlates in time with actin cytoskeleton reorganization, F-actin redistribution and stress fibers assembly followed by recovery of normal cell morphology. Presented results indicate that myosin light-chain kinase (MLCK) is responsible for the observed phosphorylation of MLC. We also found that the changes induced by P2Y₂ stimulation in actin cytoskeleton dynamics and morphology of cells with inhibited ROCK, but not in the level of phosphorylated MLC, depend on the presence of calcium in the cell environment.

Influence of cadmium ions on endothelin-1 binding and calcium signaling in rat glioma C6 cells

1995 ◽  
Vol 81 (2-3) ◽  
pp. 189-195 ◽  
Author(s):  
Klaus Koschel ◽  
Nicole N. Meissner ◽  
Piet W.L. Tas
Keyword(s):  
Calcium Signaling ◽  
C6 Cells ◽  
Cadmium Ions ◽  
Rat Glioma ◽  
Endothelin 1 ◽  
Glioma C6

Role of the actin cytoskeleton in store-mediated calcium entry in glioma C6 cells

2002 ◽  
Vol 296 (2) ◽  
pp. 484-491 ◽  
Author(s):  
Paweł Sabała ◽  
Berenika Targos ◽  
Antonella Caravelli ◽  
Rafał Czajkowski ◽  
Dmitri Lim ◽  
...  
Keyword(s):  
Actin Cytoskeleton ◽  
Calcium Entry ◽  
C6 Cells ◽  
Glioma C6

scholarly journals Modulation of ERK1/2 activity is crucial for sphingosine-induced death of glioma C6 cells.

2005 ◽  
Vol 52 (4) ◽  
pp. 927-930 ◽  
Author(s):  
Patryk Krzemiński
Keyword(s):  
Cell Death ◽  
Actin Cytoskeleton ◽  
Morphological Changes ◽  
Specific Inhibitor ◽  
Apoptotic Bodies ◽  
C6 Cells ◽  
Glioma C6 ◽  
Shed Light

In this study the contribution of the ERK1/2 pathway to sphingosine-induced death and morphological changes of the actin cytoskeleton in glioma C6 cells was investigated. Surprisingly, the level of ERK1/2 phosphorylation does not change after incubation of cells with sphingosine. Despite this, sphingosine induces rounding and detachment of cells without formation of apoptotic bodies. To shed light on this process, a specific inhibitor of ERK1/2 phosphorylation, U0126, was used. Cells incubated simultaneously with sphingosine and U0126 not only detached, but also exhibited formation of apoptotic-like blebs. These data suggest that during sphingosine-induced glioma C6 cell death apoptotic blebbing is dependent on ERK1/2 signalling and occurs only when ERK1/2 activity is decreased or abolished.

scholarly journals α-Conotoxins and α-Cobratoxin Promote, while Lipoxygenase and Cyclooxygenase Inhibitors Suppress the Proliferation of Glioma C6 Cells

Marine Drugs ◽  
2021 ◽  
Vol 19 (2) ◽  
pp. 118
Author(s):  
Tatiana I. Terpinskaya ◽  
Alexey V. Osipov ◽  
Elena V. Kryukova ◽  
Denis S. Kudryavtsev ◽  
Nina V. Kopylova ◽  
...  
Keyword(s):  
Nicotinic Acetylcholine Receptors ◽  
Acetylcholine Receptors ◽  
Glioma Cells ◽  
Nordihydroguaiaretic Acid ◽  
C6 Glioma ◽  
Cyclooxygenase Inhibitors ◽  
C6 Glioma Cells ◽  
C6 Cells ◽  
Lipoxygenase Inhibitor ◽  
Glioma C6

Among the brain tumors, glioma is the most common. In general, different biochemical mechanisms, involving nicotinic acetylcholine receptors (nAChRs) and the arachidonic acid cascade are involved in oncogenesis. Although the engagement of the latter in survival and proliferation of rat C6 glioma has been shown, there are practically no data about the presence and the role of nAChRs in C6 cells. In this work we studied the effects of nAChR antagonists, marine snail α-conotoxins and snake α-cobratoxin, on the survival and proliferation of C6 glioma cells. The effects of the lipoxygenase and cyclooxygenase inhibitors either alone or together with α-conotoxins and α-cobratoxin were studied in parallel. It was found that α-conotoxins and α-cobratoxin promoted the proliferation of C6 glioma cells, while nicotine had practically no effect at concentrations below 1 µL/mL. Nordihydroguaiaretic acid, a nonspecific lipoxygenase inhibitor, and baicalein, a 12-lipoxygenase inhibitor, exerted antiproliferative and cytotoxic effects on C6 cells. nAChR inhibitors weaken this effect after 24 h cultivation but produced no effects at longer times. Quantitative real-time polymerase chain reaction showed that mRNA for α4, α7, β2 and β4 subunits of nAChR were expressed in C6 glioma cells. This is the first indication for involvement of nAChRs in mechanisms of glioma cell proliferation.

Presence of a charybdotoxin sensitive Ca2+-activated K+ channel in rat glioma C6 cells

1988 ◽  
Vol 94 (3) ◽  
pp. 279-284 ◽  
Author(s):  
P.W.L. Tas ◽  
H.G. Kress ◽  
K. Koschel
Keyword(s):  
K Channel ◽  
C6 Cells ◽  
Rat Glioma ◽  
Glioma C6

The Role of Ca2+ and Protein Kinase C in Regulation of Phosphatidylserine Synthesis in Glioma C6 Cells

1997 ◽  
pp. 1011-1018
Author(s):  
J. Barańska ◽  
M. Czarny ◽  
P. Sabała ◽  
M. Wiktorek
Keyword(s):  
Protein Kinase C ◽  
Protein Kinase ◽  
C6 Cells ◽  
Glioma C6 ◽  
Kinase C
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