Loading…

Zinc- and Copper-Induced Interleukin-6 Release in Primary Cell Cultures From Rat Heart

The metals, zinc (Zn 2+ ) and copper (Cu 2+ ) from inhaled particulate matter may reach the systemic circulation and the cardiac tissue. In the present study, the potential of Zn 2+ and Cu 2+ to induce interleukin (IL)-6 responses in cardiomyocytes (CMs) and cardiac fibroblasts (CFs), in mono- and c...

Full description

Saved in:
Bibliographic Details
Published in:Cardiovascular toxicology 2009-06, Vol.9 (2), p.86-94
Main Authors: Ansteinsson, V., Refsnes, M., Skomedal, T., Osnes, J. B., Schiander, I., Låg, M.
Format: Article
Language:English
Subjects:
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:The metals, zinc (Zn 2+ ) and copper (Cu 2+ ) from inhaled particulate matter may reach the systemic circulation and the cardiac tissue. In the present study, the potential of Zn 2+ and Cu 2+ to induce interleukin (IL)-6 responses in cardiomyocytes (CMs) and cardiac fibroblasts (CFs), in mono- and cocultures, was examined. Both metals induced IL-6 release in a concentration (20–200 μM)-dependent manner. Zn 2+ appeared more potent than Cu 2+ in both mono- and cocultures of CMs and CFs. In the cocultures, the basal- and metal-induced IL-6 responses were synergistically increased compared to the monocultures. Exposure to Zn 2+ increased phosphorylation of the MAP-kinases, ERK1/2 and p38, in monocultures of CMs and CFs. Cu 2+ induced an increased phosphorylation of p38 in both cell types and of ERK1/2 in CFs, but at higher concentrations than Zn 2+ . Treatment with a p38 inhibitor (SB202190) reduced the IL-6 responses to Zn 2+ and Cu 2+ in both cell types. Pretreatment with PD98059 to inhibit ERK1/2 was without significant effect; however, insignificant reductions was observed in the in the CFs. In conclusion, Zn 2+ and Cu 2+ increased IL-6 release and MAP-kinase activation in primary cardiac cells, processes known to be involved in cardiac inflammation and hypertrophy.
ISSN:1530-7905
1559-0259
DOI:10.1007/s12012-009-9043-5