scholarly journals Cellular Signaling and Anti-Apoptotic Effects of Prolactin-Releasing Peptide and Its Analog on SH-SY5Y Cells

2020 ◽  
Vol 21 (17) ◽  
pp. 6343
Author(s):  
Anna Zmeškalová ◽  
Andrea Popelová ◽  
Aneta Exnerová ◽  
Blanka Železná ◽  
Jaroslav Kuneš ◽  
...  
Keyword(s):  
Protein Kinase ◽  
Signaling Pathways ◽  
Cell Line ◽  
Molecular Mechanisms ◽  
Cellular Signaling ◽  
Neuroblastoma Cell ◽  
Protein Kinase Inhibitors ◽  
Human Neuroblastoma Cell ◽  
Human Neuroblastoma ◽  
Prolactin Releasing Peptide

Prolactin-releasing peptide (PrRP), a natural ligand for the GPR10 receptor, is a neuropeptide with anorexigenic and antidiabetic properties. Due to its role in the regulation of food intake, PrRP is a potential drug for obesity treatment and associated type 2 diabetes mellitus (T2DM). Recently, the neuroprotective effects of lipidized PrRP analogs have been proven. In this study, we focused on the molecular mechanisms of action of natural PrRP31 and its lipidized analog palm11-PrRP31 in the human neuroblastoma cell line SH-SY5Y to describe their cellular signaling and possible anti-apoptotic properties. PrRP31 significantly upregulated the phosphoinositide-3 kinase-protein kinase B/Akt (PI3K-PKB/Akt) and extracellular signal-regulated kinase/cAMP response element-binding protein (ERK-CREB) signaling pathways that promote metabolic cell survival and growth. In addition, we proved via protein kinase inhibitors that activation of signaling pathways is mediated specifically by PrRP31 and its palmitoylated analog. Furthermore, the potential neuroprotective properties were studied through activation of anti-apoptotic pathways of PrRP31 and palm11-PrRP31 using the SH-SY5Y cell line and rat primary neuronal culture stressed with toxic methylglyoxal (MG). The results indicate increased viability of the cells treated with PrRP and palm11-PrRP31 and a reduced degree of apoptosis induced by MG, suggesting their potential use in the treatment of neurological disorders.

scholarly journals Neuropeptide Y modulates ATP-induced increases in internal calcium via the adenylate cyclase/protein kinase A system in a human neuroblastoma cell line

1997 ◽  
Vol 321 (2) ◽  
pp. 439-444 ◽  
Author(s):  
Virginia SOARES LEMOS ◽  
Bernard BUCHER ◽  
Kenneth TAKEDA
Keyword(s):  
Protein Kinase ◽  
Neuropeptide Y ◽  
Protein Kinase A ◽  
Cell Line ◽  
Neuroblastoma Cell ◽  
Neuroblastoma Cell Line ◽  
Human Neuroblastoma Cell ◽  
Human Neuroblastoma ◽  
Human Neuroblastoma Cell Line ◽  
Kinase A

The modulatory effects of neuropeptide Y (NPY) on ATP-induced increases in cytosolic free-calcium concentration ([Ca2+]i) were investigated in the CHP-234 human neuroblastoma cell line. Pretreatment of cells with 100 nM NPY potentiated the increase in [Ca2+]i evoked subsequently by 20 ƁM ATP, compared with initial application of ATP in a control experiment, whereas a similar pretreatment with 1 ƁM NPY attenuated the subsequent response to ATP. Both actions of NPY were completely blocked by H-89 {N-[2-((3-(4-bromo-phenyl)-2-propenyl)-amino)-ethyl]-5 isoquinoline sulphonamide dihydrochloride}, a selective antagonist of protein kinase A. The effects of 100 nM NPY were mimicked by H-89, while forskolin and 8-Br-cAMP mimicked the effects of 1 ƁM NPY. Both basal and forskolin-stimulated cAMP levels were inhibited by 100 nM NPY and by 100 nM NPY(13-36), a selective agonist of the NPY Y2-receptor subtype. In contrast, at 1 ƁM such inhibition was not observed for either NPY or NPY(13-36). It is concluded that NPY has a biphasic modulatory effect on increases in [Ca2+]i produced by ATP, which probably involves the cAMP/protein kinase A cascade.

scholarly journals Pyrido[2′,1′:2,3]imidazo[4,5-c]isoquinolin-5-amines as Potential Cytotoxic Agents against Human Neuroblastoma

2021 ◽  
Vol 14 (8) ◽  
pp. 750
Author(s):  
Zahira Tber ◽  
Mohammed Loubidi ◽  
Jabrane Jouha ◽  
Ismail Hdoufane ◽  
Mümin Alper Erdogan ◽  
...  
Keyword(s):  
Cell Line ◽  
Drug Exposure ◽  
Caspase 3 ◽  
Biological Activities ◽  
Neuroblastoma Cell ◽  
Neuroblastoma Cell Line ◽  
Cytotoxic Agents ◽  
Human Neuroblastoma Cell ◽  
Human Neuroblastoma ◽  
Parp 1

We report herein the evaluation of various pyrido[2′,1′:2,3]imidazo[4,5-c]isoquinolin-5-amines as potential cytotoxic agents. These molecules were obtained by developing the multicomponent Groebke–Blackburn–Bienaymé reaction to yield various pyrido[2′,1′:2,3]imidazo[4,5-c]quinolines which are isosteres of ellipticine whose biological activities are well established. To evaluate the anticancer potential of these pyrido[2′,1′:2,3]imidazo[4,5-c]isoquinolin-5-amine derivatives in the human neuroblastoma cell line, the cytotoxicity was examined using the WST-1 assay after 72 h drug exposure. A clonogenic assay was used to assess the ability of treated cells to proliferate and form colonies. Protein expressions (Bax, bcl-2, cleaved caspase-3, cleaved PARP-1) were analyzed using Western blotting. The colony number decrease in cells was 50.54%, 37.88% and 27.12% following exposure to compounds 2d, 2g and 4b respectively at 10 μM. We also show that treating the neuroblastoma cell line with these compounds resulted in a significant alteration in caspase-3 and PARP-1 cleavage.

scholarly journals Direct current stimulation enhances neuronal alpha-synuclein degradation in vitro

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Gessica Sala ◽  
Tommaso Bocci ◽  
Valentina Borzì ◽  
Marta Parazzini ◽  
Alberto Priori ◽  
...  
Keyword(s):  
Direct Current ◽  
Molecular Mechanisms ◽  
Neuroblastoma Cell ◽  
Alpha Synuclein ◽  
Human Neuroblastoma Cell ◽  
Human Neuroblastoma ◽  
Direct Current Stimulation ◽  
Gene And Protein Expression ◽  
Autophagic Degradation ◽  
On Line

AbstractDespite transcranial Direct Current Stimulation (DCS) is currently proposed as a symptomatic treatment in Parkinson’s disease, the intracellular and molecular mechanisms elicited by this technique are still unknown, and its disease-modifying potential unexplored. Aim of this study was to elucidate the on-line and off-line effects of DCS on the expression, aggregation and degradation of alpha-synuclein (asyn) in a human neuroblastoma cell line under basal conditions and in presence of pharmachologically-induced increased asyn levels. Following DCS, gene and protein expression of asyn and its main autophagic catabolic pathways were assessed by real-time PCR and Western blot, extracellular asyn levels by Dot blot. We found that, under standard conditions, DCS increased monomeric and reduced oligomeric asyn forms, with a concomitant down-regulation of both macroautophagy and chaperone-mediated autophagy. Differently, in presence of rotenone-induced increased asyn, DCS efficiently counteracted asyn accumulation, not acting on its gene transcription, but potentiating its degradation. DCS also reduced intracellular and extracellular asyn levels, increased following lysosomal inhibition, independently from autophagic degradation, suggesting that other mechanisms are also involved. Collectively, these findings suggest that DCS exerts on-line and off-line effects on the expression, aggregation and autophagic degradation of asyn, indicating a till unknown neuroprotective role of tDCS.

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