| First Author | Kim WK | Year | 2013 |
| Journal | PLoS One | Volume | 8 |
| Issue | 8 | Pages | e72108 |
| PubMed ID | 23977220 | Mgi Jnum | J:205835 |
| Mgi Id | MGI:5546520 | Doi | 10.1371/journal.pone.0072108 |
| Citation | Kim WK, et al. (2013) Monocyte chemoattractant protein-1 deficiency attenuates oxidative stress and protects against ovariectomy-induced chronic inflammation in mice. PLoS One 8(8):e72108 |
| abstractText | BACKGROUND: Loss of ovarian function is highly associated with an elevated risk of metabolic disease. Monocyte chemoattractant protein-1 (MCP-1, C-C chemokine ligand 2) plays critical roles in the development of inflammation, but its role in ovariectomy (OVX)-induced metabolic disturbance has not been known. METHODOLOGY AND PRINCIPAL FINDINGS: We investigated the role of MCP-1 in OVX-induced metabolic perturbation using MCP-1-knockout mice. OVX increased fat mass, serum levels of MCP-1, macrophage-colony stimulating factor (M-CSF), and reactive oxygen species (ROS), whereas MCP-1 deficiency attenuated these. OVX-induced increases of visceral fat resulted in elevated levels of highly inflammatory CD11c-expressing cells as well as other immune cells in adipose tissue, whereas a lack of MCP-1 significantly reduced all of these levels. MCP-1 deficiency attenuated activation of phospholipase Cgamma2, transforming oncogene from Ak strain, and extracellular signal-regulated kinase as well as generation of ROS, which is required for up-regulating CD11c expression upon M-CSF stimulation in bone marrow-derived macrophages. CONCLUSIONS/SIGNIFICANCE: Our data suggested that MCP-1 plays a key role in developing metabolic perturbation caused by a loss of ovarian functions through elevating CD11c expression via ROS generation. |
