z-logo
Premium
Role of MAP kinases in stress modulation of choline transport in cadmium (Cd) treated primary cultures of choroid plexus
Author(s) -
Zarate Sara M,
Stuart Samantha D Francis,
Young Robin K,
Villalobos Alice R
Publication year - 2012
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.26.1_supplement.lb761
Subject(s) - choroid plexus , stimulation , choline , kinase , mitogen activated protein kinase , p38 mitogen activated protein kinases , chemistry , microbiology and biotechnology , cytotoxicity , biochemistry , biology , endocrinology , protein kinase a , in vitro , central nervous system
Our objective is to use primary cultures of rat choroid plexus to elucidate the up‐regulation of apical choline uptake in the context of the cellular response induced by low concentrations of Cd, i.e., 250–500 nM. The roles of MAP kinases were examined in preliminary experiments. In Cd‐treated cells, ERK1/2 was activated; inhibition of ERK1/2 activation with PD98059 resulted in greater accumulation of reactive oxygen species. However, inhibition of ERK1/2 activation abated stimulation of apical 3 H‐choline uptake in Cd‐treated cells. Treatment with SP600125 to inhibit JNK activation markedly increased cytotoxicity in Cd‐treated cells as indicated by large increases in LDH release. Nevertheless, inhibition of JNK activation did not attenuate stimulation of choline uptake in Cd‐treated cells, but elicited even greater stimulation of uptake. Treatment with SB203580 to inhibit p38 MAP kinase induced a modest increase in cytotoxicity in Cd‐treated cells, but did not alter stimulation of choline uptake. These preliminary data suggest in cultured choroid plexus multiple MAP kinase pathways are activated by Cd, but stimulation of choline uptake is mediated by ERK1/2 specifically. Supported by NSF‐IOS# 1052654

This content is not available in your region!

Continue researching here.

Having issues? You can contact us here