PMID- 33075233
OWN - NLM
STAT- MEDLINE
DCOM- 20210916
LR  - 20210916
IS  - 1547-6901 (Electronic)
IS  - 1547-691X (Linking)
VI  - 17
IP  - 1
DP  - 2020 Dec
TI  - Cadmium induces CCL2 production in glioblastoma cells via activation of MAPK, 
      PI3K, and PKC pathways.
PG  - 186-193
LID - 10.1080/1547691X.2020.1829211 [doi]
AB  - Cadmium (Cd) is accumulated in human astrocytes and induces the production of 
      interleukin (IL)-6 and IL-8. Astrocytes are one of the major sources of chemokine 
      C-C motif ligand 2 (CCL2; known as monocyte chemoattractant protein-1 [MCP-1]), 
      in the brain. Elevated CCL2 levels are associated with cognitive impairment as 
      well as the migration and invasion of glioblastoma cells. The present study 
      hypothesized that non-toxic concentrations of Cd (as cadmium chloride [CdCl(2)]) 
      could up-regulate CCL2 production in U-87 MG human glio-blastoma cells. The 
      results showed that after exposure of the U-87 MG cells to CdCl(2) at 1 and 
      10 microM, there was an up-regulation of CCL2 mRNA expression after 3 h of exposure 
      and increased CCL2 secretion after 6 and 24 h. The study also found that 
      inhibition of MAPK pathways, including ERK1/2, p38, and JNK by U0126, SB203580 
      and SP600125, respectively, reduced Cd-induced CCL2 secretion by the cells. 
      Moreover, when cells were pretreated with Ro 32-0432 (an inhibitor of 
      calcium-dependent PKC) and LY294002 (a PI3K inhibitor), this also resulted in a 
      down-regulation of any Cd-induced CCL2 expression. Taken together, the results of 
      this study allow for the conclusion to be made that CCL2 up-regulation in U-87 MG 
      cells induced by Cd is mediated, in part, by an activation of MAPK, PI3K/Akt, and 
      PKC pathways.
FAU - Kasemsuk, Thitima
AU  - Kasemsuk T
AD  - Division of Pharmacology, Faculty of Pharmaceutical Sciences, Burapha University, 
      Chonburi, Thailand.
FAU - Phuagkhaopong, Suttinee
AU  - Phuagkhaopong S
AD  - Pharmacology Graduate Program, Faculty of Science, Mahidol University, Bangkok, 
      Thailand.
FAU - Yubolphan, Ruedeemars
AU  - Yubolphan R
AD  - Pharmacology Graduate Program, Faculty of Science, Mahidol University, Bangkok, 
      Thailand.
FAU - Rungreangplangkool, Norapat
AU  - Rungreangplangkool N
AD  - Faculty of Medicine Ramathibodi Hospital, Mahidol University, Bangkok, Thailand.
FAU - Vivithanaporn, Pornpun
AU  - Vivithanaporn P
AD  - Chakri Naruebodindra Medical Institute, Faculty of Medicine Ramathibodi Hospital, 
      Mahidol University, Samut Prakan, Thailand.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - England
TA  - J Immunotoxicol
JT  - Journal of immunotoxicology
JID - 101201960
RN  - 0 (CCL2 protein, human)
RN  - 0 (Chemokine CCL2)
RN  - 00BH33GNGH (Cadmium)
RN  - EC 2.7.11.13 (Protein Kinase C)
RN  - EC 2.7.11.24 (MAPK3 protein, human)
RN  - EC 2.7.11.24 (Mitogen-Activated Protein Kinase 3)
SB  - IM
MH  - Brain Neoplasms/*metabolism
MH  - Cadmium/*metabolism
MH  - Chemokine CCL2/*metabolism
MH  - Glioblastoma/*metabolism
MH  - Humans
MH  - Mitogen-Activated Protein Kinase 3
MH  - Phosphatidylinositol 3-Kinases/*metabolism
MH  - Protein Kinase C/*metabolism
MH  - Signal Transduction
OTO - NOTNLM
OT  - Akt
OT  - CCL2
OT  - Cadmium
OT  - MAPK
OT  - MCP-1
OT  - PI3K
OT  - PKC
OT  - glioblastoma
EDAT- 2020/10/20 06:00
MHDA- 2021/09/18 06:00
CRDT- 2020/10/19 20:08
PHST- 2020/10/19 20:08 [entrez]
PHST- 2020/10/20 06:00 [pubmed]
PHST- 2021/09/18 06:00 [medline]
AID - 10.1080/1547691X.2020.1829211 [doi]
PST - ppublish
SO  - J Immunotoxicol. 2020 Dec;17(1):186-193. doi: 10.1080/1547691X.2020.1829211.