Nongenomic mechanism of glucocorticoid inhibition of bradykinin-induced calcium influx in PC12 cells: Possible involvement of protein kinase C

Jian Qiu, Chen Guang Wang, Xiu Ying Huang, Yi Zhang Chen

Research output: Contribution to journalArticle

33 Citations (Scopus)

Abstract

Many stimulants, including bradykinin (BK), can induce increase in [Ca2+]i in PC12 cells. Bradykinin induces an increase in [Ca2+]i via intracellular Ca2+ release and extracellular Ca2+ influx through the transduction of G protein, but not through voltage-sensitive calcium channels. In this experiment, We analyzed how corticosterone (Cort) influences BK-induced intracellular Ca2+ release and extracellular Ca2+ influx, and further studied the mechanism of glucocorticoid's action. To dissociate the intracellular Ca2+ release and extracellular Ca2+ influx induced by BK, the Ca2+-free/Ca2+- reintroduction protocol was used. The results were as follows: (1) The Ca2+ influx induced by BK could be rapidly inhibited by Cort, but intracellular Ca2+ release could not be affected significantly. (2) The inhibitory effect of Cort-BSA (BSA -conjugated Cort) on Ca2+ influx induced by BK was the same as the effect of free Cort. (3) Protein kinase C (PKC) activator (phorbol 12-myristate 13-acetate) could mimic and PKC inhibitor Gö6976 could reverse the inhibitory effect of Cort. (4) There was no inhibitory effect of Cort on Ca2+ influx induced by BK when pretreated with pertussis toxin. The results suggested, for the first time, that Cort might act via a putative membrane receptor and inhibit the Ca2+ influx induced by BK through the pertussis toxin -sensitive G protein-PKC pathway.

Original languageEnglish (US)
Pages (from-to)2533-2542
Number of pages10
JournalLife Sciences
Volume72
Issue number22
DOIs
StatePublished - Apr 18 2003
Externally publishedYes

Fingerprint

PC12 Cells
Bradykinin
Corticosterone
Protein Kinase C
Glucocorticoids
Calcium
Pertussis Toxin
GTP-Binding Proteins
Protein C Inhibitor
Calcium Channels
Protein Kinase Inhibitors
Acetates
Membranes
Electric potential

Keywords

  • Bradykinin
  • Ca
  • Corticosterone
  • G-protein
  • Nongenomic
  • PC12 cells
  • PKC

ASJC Scopus subject areas

  • Pharmacology

Cite this

Nongenomic mechanism of glucocorticoid inhibition of bradykinin-induced calcium influx in PC12 cells : Possible involvement of protein kinase C. / Qiu, Jian; Wang, Chen Guang; Huang, Xiu Ying; Chen, Yi Zhang.

In: Life Sciences, Vol. 72, No. 22, 18.04.2003, p. 2533-2542.

Research output: Contribution to journalArticle

@article{f62d50d953cd4ea09a4077abcc53aa81,
title = "Nongenomic mechanism of glucocorticoid inhibition of bradykinin-induced calcium influx in PC12 cells: Possible involvement of protein kinase C",
abstract = "Many stimulants, including bradykinin (BK), can induce increase in [Ca2+]i in PC12 cells. Bradykinin induces an increase in [Ca2+]i via intracellular Ca2+ release and extracellular Ca2+ influx through the transduction of G protein, but not through voltage-sensitive calcium channels. In this experiment, We analyzed how corticosterone (Cort) influences BK-induced intracellular Ca2+ release and extracellular Ca2+ influx, and further studied the mechanism of glucocorticoid's action. To dissociate the intracellular Ca2+ release and extracellular Ca2+ influx induced by BK, the Ca2+-free/Ca2+- reintroduction protocol was used. The results were as follows: (1) The Ca2+ influx induced by BK could be rapidly inhibited by Cort, but intracellular Ca2+ release could not be affected significantly. (2) The inhibitory effect of Cort-BSA (BSA -conjugated Cort) on Ca2+ influx induced by BK was the same as the effect of free Cort. (3) Protein kinase C (PKC) activator (phorbol 12-myristate 13-acetate) could mimic and PKC inhibitor G{\"o}6976 could reverse the inhibitory effect of Cort. (4) There was no inhibitory effect of Cort on Ca2+ influx induced by BK when pretreated with pertussis toxin. The results suggested, for the first time, that Cort might act via a putative membrane receptor and inhibit the Ca2+ influx induced by BK through the pertussis toxin -sensitive G protein-PKC pathway.",
keywords = "Bradykinin, Ca, Corticosterone, G-protein, Nongenomic, PC12 cells, PKC",
author = "Jian Qiu and Wang, {Chen Guang} and Huang, {Xiu Ying} and Chen, {Yi Zhang}",
year = "2003",
month = "4",
day = "18",
doi = "10.1016/S0024-3205(03)00168-1",
language = "English (US)",
volume = "72",
pages = "2533--2542",
journal = "Life Sciences",
issn = "0024-3205",
publisher = "Elsevier Inc.",
number = "22",

}

TY - JOUR

T1 - Nongenomic mechanism of glucocorticoid inhibition of bradykinin-induced calcium influx in PC12 cells

T2 - Possible involvement of protein kinase C

AU - Qiu, Jian

AU - Wang, Chen Guang

AU - Huang, Xiu Ying

AU - Chen, Yi Zhang

PY - 2003/4/18

Y1 - 2003/4/18

N2 - Many stimulants, including bradykinin (BK), can induce increase in [Ca2+]i in PC12 cells. Bradykinin induces an increase in [Ca2+]i via intracellular Ca2+ release and extracellular Ca2+ influx through the transduction of G protein, but not through voltage-sensitive calcium channels. In this experiment, We analyzed how corticosterone (Cort) influences BK-induced intracellular Ca2+ release and extracellular Ca2+ influx, and further studied the mechanism of glucocorticoid's action. To dissociate the intracellular Ca2+ release and extracellular Ca2+ influx induced by BK, the Ca2+-free/Ca2+- reintroduction protocol was used. The results were as follows: (1) The Ca2+ influx induced by BK could be rapidly inhibited by Cort, but intracellular Ca2+ release could not be affected significantly. (2) The inhibitory effect of Cort-BSA (BSA -conjugated Cort) on Ca2+ influx induced by BK was the same as the effect of free Cort. (3) Protein kinase C (PKC) activator (phorbol 12-myristate 13-acetate) could mimic and PKC inhibitor Gö6976 could reverse the inhibitory effect of Cort. (4) There was no inhibitory effect of Cort on Ca2+ influx induced by BK when pretreated with pertussis toxin. The results suggested, for the first time, that Cort might act via a putative membrane receptor and inhibit the Ca2+ influx induced by BK through the pertussis toxin -sensitive G protein-PKC pathway.

AB - Many stimulants, including bradykinin (BK), can induce increase in [Ca2+]i in PC12 cells. Bradykinin induces an increase in [Ca2+]i via intracellular Ca2+ release and extracellular Ca2+ influx through the transduction of G protein, but not through voltage-sensitive calcium channels. In this experiment, We analyzed how corticosterone (Cort) influences BK-induced intracellular Ca2+ release and extracellular Ca2+ influx, and further studied the mechanism of glucocorticoid's action. To dissociate the intracellular Ca2+ release and extracellular Ca2+ influx induced by BK, the Ca2+-free/Ca2+- reintroduction protocol was used. The results were as follows: (1) The Ca2+ influx induced by BK could be rapidly inhibited by Cort, but intracellular Ca2+ release could not be affected significantly. (2) The inhibitory effect of Cort-BSA (BSA -conjugated Cort) on Ca2+ influx induced by BK was the same as the effect of free Cort. (3) Protein kinase C (PKC) activator (phorbol 12-myristate 13-acetate) could mimic and PKC inhibitor Gö6976 could reverse the inhibitory effect of Cort. (4) There was no inhibitory effect of Cort on Ca2+ influx induced by BK when pretreated with pertussis toxin. The results suggested, for the first time, that Cort might act via a putative membrane receptor and inhibit the Ca2+ influx induced by BK through the pertussis toxin -sensitive G protein-PKC pathway.

KW - Bradykinin

KW - Ca

KW - Corticosterone

KW - G-protein

KW - Nongenomic

KW - PC12 cells

KW - PKC

UR - http://www.scopus.com/inward/record.url?scp=0345700743&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0345700743&partnerID=8YFLogxK

U2 - 10.1016/S0024-3205(03)00168-1

DO - 10.1016/S0024-3205(03)00168-1

M3 - Article

C2 - 12650862

AN - SCOPUS:0345700743

VL - 72

SP - 2533

EP - 2542

JO - Life Sciences

JF - Life Sciences

SN - 0024-3205

IS - 22

ER -