5-HT2A serotonin receptor agonist DOI alleviates cytotoxicity in neuroblastoma cells: Role of the ERK pathway

2013 ◽  
Vol 44 ◽  
pp. 64-72 ◽  
Author(s):  
Zoya Marinova ◽  
Susanne Walitza ◽  
Edna Grünblatt
Keyword(s):  
Receptor Agonist ◽  
Serotonin Receptor ◽  
Neuroblastoma Cells ◽  
Erk Pathway

scholarly journals Role of some types of serotonin receptors in murine hypophyseal-testicular complex activation induced by the presence of a female

2003 ◽  
Vol 49 (6) ◽  
pp. 53-56
Author(s):  
T. G. Amstislavskaya ◽  
N. K. Popova
Keyword(s):  
Serotonin Receptors ◽  
Receptor Agonist ◽  
Serotonin Receptor ◽  
Receptive Female ◽  
Plasma Testosterone ◽  
Blood Levels ◽  
Inhibitory Effects ◽  
Sexual Activation ◽  
Different Types

Placement of a sexually receptive female mouse behind a partition that prevents physical contacts, but permits it to see and smell caused an increase in the blood levels of testosterone in male mice. The selective 5-HTIA-serotonin receptor agonist 08-OH- DPAT (0.1 mg/kg) and the mixed 5-HTIA/IB agonist eltoprazine, 3.0 and 10.0 mg/kg, blocked the activating effect of female exposure on the male pituitary-testicular system. The 5-HT/-receptor agonist p-MPPI (0.2 mg/kg) prevented the inhibitory effects of 8-OH-DPATand eltoprazine. The 5-HT/B-receptor agonist CGS- 12066A (1.0 and 2.0 mg/kg) exerted no effect while the mixed 5-HTIB/2C-receptor agonist TFMPP (5.2 mg/kg) inhibited a female-induced increase in the levels of male blood testosterone. The 5-HT/-receptor agonist keranserin (1.0 and 2.0 mg/kg) prevented a female-induced increase in the levels of testosterone. The 5-HT3-receptor agonist ondansetron (0.05 and 0.1 mg/kg) elevated the baseline level of plasma testosterone, but blocked receptive female-induced activation of the male hypothalamic-pituitary-testicular system (HPTS). It is concluded that 5-HTIA-receptors are involved in the control of male sexual activation. At the same time different types and even subtypes of the same type of 5-HT-receptors produce varying inhibitory and activating effects on the receptive female-induced activation of HPTS. Blocking of the female-induced activation of HPTS seems to be realized by involving 5-HTu- and 5-HT2C-receptors and its activation occurs with the participation of 5-HT^- and 5- HT3-receptors.

Role of 5-HT2B Serotonin Receptor Agonist in the Regulation of Pumping Function of the Heart

2015 ◽  
Vol 159 (3) ◽  
pp. 302-304 ◽  
Author(s):  
R. A. Abzalov ◽  
A. M. Valeev ◽  
N. I. Abzalov ◽  
A. A. Gulyakov
Keyword(s):  
Receptor Agonist ◽  
Serotonin Receptor ◽  
Pumping Function

Assessment for the Role of Serotonin Receptor Subtype 3 for the Analgesic Action of Morphine at the Spinal Level

2005 ◽  
Vol 18 (2) ◽  
pp. 113
Author(s):  
Myung Ha Yoon ◽  
Hong Buem Bae ◽  
Jeong Il Choi ◽  
Seok Jae Kim ◽  
Chang Mo Kim ◽  
...  
Keyword(s):  
Serotonin Receptor ◽  
Receptor Subtype ◽  
Analgesic Action ◽  
Spinal Level ◽  
Subtype 3

scholarly journals Loss of RET Promotes Mesenchymal Identity in Neuroblastoma Cells

Cancers ◽  
2021 ◽  
Vol 13 (8) ◽  
pp. 1909
Author(s):  
Joachim T. Siaw ◽  
Jonatan L. Gabre ◽  
Ezgi Uçkun ◽  
Marc Vigny ◽  
Wancun Zhang ◽  
...  
Keyword(s):  
Genome Engineering ◽  
Neuroblastoma Cells ◽  
Gene Signature ◽  
Additional Insight ◽  
Downstream Target ◽  
Anaplastic Lymphoma ◽  
Extracellular Matrix Components ◽  
Transforming Gene ◽  
Insight Into

Aberrant activation of anaplastic lymphoma kinase (ALK) drives neuroblastoma (NB). Previous work identified the RET receptor tyrosine kinase (RTK) as a downstream target of ALK activity in NB models. We show here that ALK activation in response to ALKAL2 ligand results in the rapid phosphorylation of RET in NB cells, providing additional insight into the contribution of RET to the ALK-driven gene signature in NB. To further address the role of RET in NB, RET knockout (KO) SK-N-AS cells were generated by CRISPR/Cas9 genome engineering. Gene expression analysis of RET KO NB cells identified a reprogramming of NB cells to a mesenchymal (MES) phenotype that was characterized by increased migration and upregulation of the AXL and MNNG HOS transforming gene (MET) RTKs, as well as integrins and extracellular matrix components. Strikingly, the upregulation of AXL in the absence of RET reflects the development timeline observed in the neural crest as progenitor cells undergo differentiation during embryonic development. Together, these findings suggest that a MES phenotype is promoted in mesenchymal NB cells in the absence of RET, reflective of a less differentiated developmental status.

Regulation of intracellular calcium in N1E-115 neuroblastoma cells: the role of Na+/Ca2+exchange

2002 ◽  
Vol 282 (5) ◽  
pp. C1000-C1008 ◽  
Author(s):  
Kara L. Kopper ◽  
Joseph S. Adorante
Keyword(s):  
Membrane Potential ◽  
Intracellular Calcium ◽  
Normal Cell ◽  
Buffer Capacity ◽  
Neuroblastoma Cells ◽  
Fold Increase ◽  
Scorpion Venom ◽  
Reverse Mode ◽  
Intracellular Ca

In fura 2-loaded N1E-115 cells, regulation of intracellular Ca2+ concentration ([Ca2+]i) following a Ca2+ load induced by 1 μM thapsigargin and 10 μM carbonylcyanide p-trifluoromethyoxyphenylhydrazone (FCCP) was Na+ dependent and inhibited by 5 mM Ni2+. In cells with normal intracellular Na+ concentration ([Na+]i), removal of bath Na+, which should result in reversal of Na+/Ca2+exchange, did not increase [Ca2+]i unless cell Ca2+ buffer capacity was reduced. When N1E-115 cells were Na+ loaded using 100 μM veratridine and 4 μg/ml scorpion venom, the rate of the reverse mode of the Na+/Ca2+ exchanger was apparently enhanced, since an ∼4- to 6-fold increase in [Ca2+]ioccurred despite normal cell Ca2+ buffering. In SBFI-loaded cells, we were able to demonstrate forward operation of the Na+/Ca2+ exchanger (net efflux of Ca2+) by observing increases (∼ 6 mM) in [Na+]i. These Ni2+ (5 mM)-inhibited increases in [Na+]i could only be observed when a continuous ionomycin-induced influx of Ca2+ occurred. The voltage-sensitive dye bis-(1,3-diethylthiobarbituric acid) trimethine oxonol was used to measure changes in membrane potential. Ionomycin (1 μM) depolarized N1E-115 cells (∼25 mV). This depolarization was Na+dependent and blocked by 5 mM Ni2+ and 250–500 μM benzamil. These data provide evidence for the presence of an electrogenic Na+/Ca2+ exchanger that is capable of regulating [Ca2+]i after release of Ca2+ from cell stores.

scholarly journals The oncogene BRAFV600E is associated with a high risk of recurrence and less differentiated papillary thyroid carcinoma due to the impairment of Na+/I− targeting to the membrane

2006 ◽  
Vol 13 (1) ◽  
pp. 257-269 ◽  
Author(s):  
G Riesco-Eizaguirre ◽  
P Gutiérrez-Martínez ◽  
M A García-Cabezas ◽  
M Nistal ◽  
P Santisteban
Keyword(s):  
High Risk ◽  
Papillary Thyroid Carcinoma ◽  
Thyroid Carcinoma ◽  
Prognostic Impact ◽  
Erk Pathway ◽  
Papillary Thyroid ◽  
Thyroid Cells ◽  
Genetic Event ◽  
Total Body

The oncogene BRAFV600E is the most frequent genetic event in papillary thyroid carcinoma (PTC) but its prognostic impact still remains to be elucidated. We evaluated a representative series of 67 individuals with PTC who underwent total thyroidectomy. BRAF-positive tumours correlated with early recurrences (32% vs 7.6%; P=0.02) during a median postoperative follow-up period of 3 years. Interestingly, within the recurrences, a significant majority had negative radioiodine (131I) total body scans, predicting a poorer outcome as treatment with 131I is not effective. This last observation led us to investigate the role of BRAFV600E and the MEK-ERK pathway in thyroid dedifferentiation, particularly in Na+/I− symporter (NIS) impairment, as this thyroid-specific plasma membrane glycoprotein mediates active transport of I− into the thyroid follicular cells. A subset of 60 PTC samples was evaluated for NIS immunoreactivity and, accordingly, we confirmed a significant low NIS expression and impaired targeting to membranes in BRAF-positive samples (3.5% vs 30%; P=0.005). Furthermore, experiments with differentiated PCCl3 thyroid cells demonstrated that transient expression of BRAFV600E sharply impaired both NIS expression and targeting to membrane and, surprisingly, this impairment was not totally dependent on the MEK-ERK pathway. We have concluded that BRAFV600E is a new prognostic factor in PTC that correlates with a high risk of recurrences and less differentiated tumours due to the loss of NIS-mediated 131I uptake.

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