Effects of pituitary adenylate cyclase activating polypeptide on the survival and signal transduction pathways in human choriocarcinoma cells

Research output: Chapter in Book/Report/Conference proceedingConference contribution

10 Citations (Scopus)

Abstract

The pituitary adenylate cyclase activating polypeptide (PACAP) has several effects in endocrine and reproductive organs, including the placenta. PACAP is generally known as a survival-promoting peptide acting on divergent signal transduction pathways. However, its effects on the survival and signaling mechanisms of trophoblast cells are not known. In the present study we found that 1-h pretreatment with PACAP38 did not significantly influence the survival of JAR cytotrophoblast cells. However, the survival rate of cells exposed to oxidative stress or CoCl2-induced in vitro hypoxia showed a significant further decrease in PACAP-treated cells, implying that PACAP sensitizes the cells to these stressors. This was not observed in the case of lipopolysaccharide or ethanol treatment. Western blot data revealed that, in cells exposed to oxidative stress, PACAP treatment decreased phosphorylation of all extracellular signal-regulated kinase (ERK), phospho-jun N-terminal kinase (JNK), protein kinase B, p38 mitogen-activated protein kinase (MAPK), and phospho-glycogen synthase kinase (GSK) and the expression of bax. The overall effect seems to be a sensitizing effect in almost all examined pathways when oxidative stress was applied, which may explain the enhancing effect of PACAP on cell death in contrast to most other cell types examined so far. Our data show that the signaling mechanism of PACAP may be different in trophoblast cells to that observed in other cell lines.

Original languageEnglish
Title of host publicationAnnals of the New York Academy of Sciences
Pages353-357
Number of pages5
Volume1163
DOIs
Publication statusPublished - Apr 2009

Publication series

NameAnnals of the New York Academy of Sciences
Volume1163
ISSN (Print)00778923
ISSN (Electronic)17496632

Fingerprint

Pituitary Adenylate Cyclase-Activating Polypeptide
Signal transduction
Choriocarcinoma
Signal Transduction
Survival
Oxidative stress
Trophoblasts
Oxidative Stress
Cells
Glycogen Synthase Kinases
Proto-Oncogene Proteins c-akt
Phosphorylation
Extracellular Signal-Regulated MAP Kinases
p38 Mitogen-Activated Protein Kinases
Cell death
Placenta
Lipopolysaccharides
Cell Death
Ethanol
Phosphotransferases

Keywords

  • Akt
  • Bax
  • ERK
  • GSK
  • JNK
  • P38 MAPK
  • Trophoblast

ASJC Scopus subject areas

  • Biochemistry, Genetics and Molecular Biology(all)

Cite this

Effects of pituitary adenylate cyclase activating polypeptide on the survival and signal transduction pathways in human choriocarcinoma cells. / Boronkai, A.; Brubel, R.; Rácz, B.; Tamás, A.; Kiss, P.; Horvath, G.; Lubics, A.; Szigeti, A.; Bellyei, S.; Tóth, G.; Lakatos, A.; Reglodi, D.

Annals of the New York Academy of Sciences. Vol. 1163 2009. p. 353-357 (Annals of the New York Academy of Sciences; Vol. 1163).

Research output: Chapter in Book/Report/Conference proceedingConference contribution

Boronkai A, Brubel R, Rácz B, Tamás A, Kiss P, Horvath G et al. Effects of pituitary adenylate cyclase activating polypeptide on the survival and signal transduction pathways in human choriocarcinoma cells. In Annals of the New York Academy of Sciences. Vol. 1163. 2009. p. 353-357. (Annals of the New York Academy of Sciences). https://doi.org/10.1111/j.1749-6632.2008.03630.x
@inproceedings{35499afd3dca468e97aa1f9a083a62e5,
title = "Effects of pituitary adenylate cyclase activating polypeptide on the survival and signal transduction pathways in human choriocarcinoma cells",
abstract = "The pituitary adenylate cyclase activating polypeptide (PACAP) has several effects in endocrine and reproductive organs, including the placenta. PACAP is generally known as a survival-promoting peptide acting on divergent signal transduction pathways. However, its effects on the survival and signaling mechanisms of trophoblast cells are not known. In the present study we found that 1-h pretreatment with PACAP38 did not significantly influence the survival of JAR cytotrophoblast cells. However, the survival rate of cells exposed to oxidative stress or CoCl2-induced in vitro hypoxia showed a significant further decrease in PACAP-treated cells, implying that PACAP sensitizes the cells to these stressors. This was not observed in the case of lipopolysaccharide or ethanol treatment. Western blot data revealed that, in cells exposed to oxidative stress, PACAP treatment decreased phosphorylation of all extracellular signal-regulated kinase (ERK), phospho-jun N-terminal kinase (JNK), protein kinase B, p38 mitogen-activated protein kinase (MAPK), and phospho-glycogen synthase kinase (GSK) and the expression of bax. The overall effect seems to be a sensitizing effect in almost all examined pathways when oxidative stress was applied, which may explain the enhancing effect of PACAP on cell death in contrast to most other cell types examined so far. Our data show that the signaling mechanism of PACAP may be different in trophoblast cells to that observed in other cell lines.",
keywords = "Akt, Bax, ERK, GSK, JNK, P38 MAPK, Trophoblast",
author = "A. Boronkai and R. Brubel and B. R{\'a}cz and A. Tam{\'a}s and P. Kiss and G. Horvath and A. Lubics and A. Szigeti and S. Bellyei and G. T{\'o}th and A. Lakatos and D. Reglodi",
year = "2009",
month = "4",
doi = "10.1111/j.1749-6632.2008.03630.x",
language = "English",
isbn = "9781573316712",
volume = "1163",
series = "Annals of the New York Academy of Sciences",
pages = "353--357",
booktitle = "Annals of the New York Academy of Sciences",

}

TY - GEN

T1 - Effects of pituitary adenylate cyclase activating polypeptide on the survival and signal transduction pathways in human choriocarcinoma cells

AU - Boronkai, A.

AU - Brubel, R.

AU - Rácz, B.

AU - Tamás, A.

AU - Kiss, P.

AU - Horvath, G.

AU - Lubics, A.

AU - Szigeti, A.

AU - Bellyei, S.

AU - Tóth, G.

AU - Lakatos, A.

AU - Reglodi, D.

PY - 2009/4

Y1 - 2009/4

N2 - The pituitary adenylate cyclase activating polypeptide (PACAP) has several effects in endocrine and reproductive organs, including the placenta. PACAP is generally known as a survival-promoting peptide acting on divergent signal transduction pathways. However, its effects on the survival and signaling mechanisms of trophoblast cells are not known. In the present study we found that 1-h pretreatment with PACAP38 did not significantly influence the survival of JAR cytotrophoblast cells. However, the survival rate of cells exposed to oxidative stress or CoCl2-induced in vitro hypoxia showed a significant further decrease in PACAP-treated cells, implying that PACAP sensitizes the cells to these stressors. This was not observed in the case of lipopolysaccharide or ethanol treatment. Western blot data revealed that, in cells exposed to oxidative stress, PACAP treatment decreased phosphorylation of all extracellular signal-regulated kinase (ERK), phospho-jun N-terminal kinase (JNK), protein kinase B, p38 mitogen-activated protein kinase (MAPK), and phospho-glycogen synthase kinase (GSK) and the expression of bax. The overall effect seems to be a sensitizing effect in almost all examined pathways when oxidative stress was applied, which may explain the enhancing effect of PACAP on cell death in contrast to most other cell types examined so far. Our data show that the signaling mechanism of PACAP may be different in trophoblast cells to that observed in other cell lines.

AB - The pituitary adenylate cyclase activating polypeptide (PACAP) has several effects in endocrine and reproductive organs, including the placenta. PACAP is generally known as a survival-promoting peptide acting on divergent signal transduction pathways. However, its effects on the survival and signaling mechanisms of trophoblast cells are not known. In the present study we found that 1-h pretreatment with PACAP38 did not significantly influence the survival of JAR cytotrophoblast cells. However, the survival rate of cells exposed to oxidative stress or CoCl2-induced in vitro hypoxia showed a significant further decrease in PACAP-treated cells, implying that PACAP sensitizes the cells to these stressors. This was not observed in the case of lipopolysaccharide or ethanol treatment. Western blot data revealed that, in cells exposed to oxidative stress, PACAP treatment decreased phosphorylation of all extracellular signal-regulated kinase (ERK), phospho-jun N-terminal kinase (JNK), protein kinase B, p38 mitogen-activated protein kinase (MAPK), and phospho-glycogen synthase kinase (GSK) and the expression of bax. The overall effect seems to be a sensitizing effect in almost all examined pathways when oxidative stress was applied, which may explain the enhancing effect of PACAP on cell death in contrast to most other cell types examined so far. Our data show that the signaling mechanism of PACAP may be different in trophoblast cells to that observed in other cell lines.

KW - Akt

KW - Bax

KW - ERK

KW - GSK

KW - JNK

KW - P38 MAPK

KW - Trophoblast

UR - http://www.scopus.com/inward/record.url?scp=65449125890&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=65449125890&partnerID=8YFLogxK

U2 - 10.1111/j.1749-6632.2008.03630.x

DO - 10.1111/j.1749-6632.2008.03630.x

M3 - Conference contribution

C2 - 19456358

AN - SCOPUS:65449125890

SN - 9781573316712

VL - 1163

T3 - Annals of the New York Academy of Sciences

SP - 353

EP - 357

BT - Annals of the New York Academy of Sciences

ER -