Effects of Prolactin on Ionic Membrane Conductances in the Human Malignant Astrocytoma Cell Line U87-MG

2004 ◽  
Vol 91 (3) ◽  
pp. 1203-1216 ◽  
Author(s):  
Thomas Ducret ◽  
Anne-Marie Vacher ◽  
Pierre Vacher
Keyword(s):  
Cell Membrane ◽  
Cell Line ◽  
Malignant Astrocytoma ◽  
Patch Clamp Technique ◽  
Peripheral Tissues ◽  
Membrane Hyperpolarization ◽  
Membrane Conductances ◽  
Astrocytoma Cell Line ◽  
Astrocytoma Cell ◽  
Ion Conductances

Prolactin (PRL) is involved in numerous biological processes in peripheral tissues and the brain. Although numerous studies have been conducted to elucidate the signal transduction pathways associated with the PRL receptor, very few have examined the role of ion conductances in PRL actions. We used the patch-clamp technique in “whole cell” configuration and microspectrofluorimetry to investigate the effects of PRL on membrane ion conductances in the U87-MG human malignant astrocytoma cell line, which naturally expresses the PRL receptor. We found that a physiological concentration (4 nM) of PRL exerted a biphasic action on membrane conductances. First, PRL activated a Ca2+-dependent K+ current that was sensitive to CTX and TEA. This current depended on PRL-induced Ca2+ mobilization, through a JAK2-dependent pathway from a thapsigargin- and 2-APB-sensitive Ca2+ pool. Second, PRL also activated an inwardly directed current, mainly due to the stimulation of calcium influx via nickel- and 2-APB-sensitive calcium channels. Both phases resulted in membrane hyperpolarizations, mainly through the activation of Ca2+-dependent K+ channels. As shown by combined experiments (electrophysiology and microspectrofluorimetry), the PRL-induced Ca2+ influx increased with cell membrane hyperpolarization and conversely decreased with cell membrane depolarization. Thus PRL-induced membrane hyperpolarizations facilitated Ca2+ influx through voltage-independent Ca2+ channels. Finally, PRL also activated a DIDS-sensitive Cl- current, which may participate in the PRL-induced hyperpolarization. These PRL-induced conductance activations are probably related to the PRL proliferative effect we have already described in U87-MG cells.

Establishment and characterization of a novel malignant astrocytoma cell line derived from a tumor removed in a patient with neurofibromatosis Type 1

2001 ◽  
Vol 94 (2) ◽  
pp. 301-308 ◽  
Author(s):  
Masanori Kurimoto ◽  
Yutaka Hirashima ◽  
Tsuneaki Ogiichi ◽  
Hideo Hamada ◽  
Hironaga Kamiyama ◽  
...  
Keyword(s):  
Cell Line ◽  
Neurofibromatosis Type 1 ◽  
Proliferative Activity ◽  
Neurofibromatosis Type ◽  
Malignant Astrocytoma ◽  
Content Type ◽  
Astrocytoma Cell Line ◽  
Astrocytoma Cell ◽  
Fine Print

Object. Patients with neurofibromatosis Type 1 (NF1) have a predisposition to development of a variety of benign and malignant tumors including neurofibromas, astrocytomas, pheochromocytomas, and malignant peripheral nerve sheath tumors. The availability of an astrocytoma cell line derived from NF1 would be useful in studies in which sporadic astrocytomas could be compared with NF1-derived astrocytomas. In this article the authors describe a novel astrocytoma cell line, TM-31, that they established from a tumor removed in a 42-year-old woman with NF1. Methods. The TM-31 cell line was prepared from a surgical specimen of malignant astrocytoma and was serially subcultured over 250 times throughout a 6-year period without showing any sign of cell senescence. Immunocytochemical analyses demonstrated that TM-31 cells are negative for glial fibrillary acidic protein but positive for vimentin and S-100 protein. The TM-31 cells display little neurofibromin expression when subjected to immunoblotting, indicating that there is an NF1 gene mutation. Polymerase chain reaction—single-strand conformational polymorphism analysis revealed that TM-31 cells harbor a p53 point mutation in exon 7, codon 238. Chemosensitivity testing of TM-31 cells revealed a resistance to 1-(4-amino-2-methyl-5-pyrimidinyl)methyl-3-(2-chloroethyl)-3-nitrosourea, although they are sensitive to cisplatin and etoposide. In addition, TM-31 cells displayed no morphological differentiation after all-transretinoic acid and dibutyryl cyclic adenosine monophosphate treatments. Pharmacological inhibition of farnesyltransferase of the Ras oncoprotein led to decreased proliferative activity and inhibition of anchorage-independent growth of TM-31 cells in soft agar. Conclusions. The TM-31 cell line is an immortalized astrocytoma cell line derived from a tumor obtained in a patient with NF1. Ras activation may be the major event of proliferative activity and of the transformed phenotype of TM-31 cells, and the farnesyltransferase inhibitor may be potentially important as a novel antiproliferative therapy for NF1-derived astrocytomas.

scholarly journals Sulfatide-Rich Liposome Uptake by a Human-Derived Neuroblastoma Cell Line

Processes ◽  
2020 ◽  
Vol 8 (12) ◽  
pp. 1615
Author(s):  
Daniel Arroyo-Ariza ◽  
Elizabeth Suesca ◽  
Chad Leidy ◽  
John M. Gonzalez
Keyword(s):  
Cell Membrane ◽  
Cell Line ◽  
Targeted Delivery ◽  
Neuroblastoma Cell ◽  
Density Lipoprotein ◽  
Chemotherapeutic Agents ◽  
Neuroblastoma Cell Line ◽  
Endocytic Pathway ◽  
Astrocytoma Cell Line ◽  
Astrocytoma Cell

Liposomes are bilayer membrane vesicles that can serve as vehicles for drug delivery. They are a good alternative to free drug administration that provides cell-targeted delivery into tumors, limiting the systemic toxicity of chemotherapeutic agents. Previous results from our group showed that an astrocytoma cell line exhibits selective uptake of sulfatide-rich (SCB) liposomes, mediated by the low-density lipoprotein receptor (LDL-R). The goal of this study was to assess the uptake of liposomes in a neuroblastoma cell line. For this purpose, we used two types of liposomes, one representing a regular cell membrane (DOPC) and another rich in myelin components (SCB). An astrocytoma cell line was used as a control. Characterization of liposome uptake and distribution was conducted by flow cytometry and fluorescence microscopy. Similar levels of LDL-R expression were found in both cell lines. The uptake of SCB liposomes was higher than that of DOPC liposomes. No alterations in cell viability were found. SCB liposomes were located near the cell membrane and did not colocalize within the acidic cellular compartments. Two endocytic pathway inhibitors did not affect the liposome uptake. Neuroblastoma cells exhibited a similar uptake of SCB liposomes as astrocytoma cells; however, the pathway involved appeared to be different than the hypothesized pathway of LDL-R clathrin-mediated endocytosis.

scholarly journals Post-transcriptional regulation of fukutin in an astrocytoma cell line

2012 ◽  
Vol 93 (1) ◽  
pp. 46-55 ◽  
Author(s):  
Tomoko Yamamoto ◽  
Yoichiro Kato ◽  
Atsuko Hiroi ◽  
Noriyuki Shibata ◽  
Makiko Osawa ◽  
...  
Keyword(s):  
Transcriptional Regulation ◽  
Cell Line ◽  
Astrocytoma Cell Line ◽  
Astrocytoma Cell ◽  
Post Transcriptional Regulation

scholarly journals Pathways of 4-Hydroxy-2-Nonenal Detoxification in a Human Astrocytoma Cell Line

Antioxidants ◽  
2020 ◽  
Vol 9 (5) ◽  
pp. 385
Author(s):  
Eleonora Peroni ◽  
Viola Scali ◽  
Francesco Balestri ◽  
Mario Cappiello ◽  
Umberto Mura ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cell Line ◽  
Reducing Power ◽  
Astrocytoma Cell Line ◽  
Astrocytoma Cell ◽  
Human Astrocytoma ◽  
Lens Cell ◽  
High Level ◽  
Human Astrocytoma Cell Line ◽  
Better Than

One of the consequences of the increased level of oxidative stress that often characterizes the cancer cell environment is the abnormal generation of lipid peroxidation products, above all 4-hydroxynonenal. The contribution of this aldehyde to the pathogenesis of several diseases is well known. In this study, we characterized the ADF astrocytoma cell line both in terms of its pattern of enzymatic activities devoted to 4-hydroxynonenal removal and its resistance to oxidative stress induced by exposure to hydrogen peroxide. A comparison with lens cell lines, which, due to the ocular function, are normally exposed to oxidative conditions is reported. Our results show that, overall, ADF cells counteract oxidative stress conditions better than normal cells, thus confirming the redox adaptation demonstrated for several cancer cells. In addition, the markedly high level of NADP+-dependent dehydrogenase activity acting on the glutahionyl-hydroxynonanal adduct detected in ADF cells may promote, at the same time, the detoxification and recovery of cell-reducing power in these cells.

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