Role of MCP-1 and MIP-1α in retinal neovascularization during postischemic inflammation in a mouse model of retinal neovascularization

Shigeo Yoshida, Ayako Yoshida, Tatsuro Ishibashi, Susan G. Elner, Victor M. Elner

Research output: Contribution to journalArticle

121 Citations (Scopus)

Abstract

Macrophages are important participants in neovascularization. This study was designed to examine the role of the monocyte/macrophage chemotactic proteins, monocyte chemotactic protein-1 (MCP-1), and macrophage inflammatory protein-1α (MIP-1α) in a mouse model of oxygen-induced ischemic retinopathy and to determine whether the morphology and distribution of macrophages/microglia are concomitantly altered. The MCP-1, MIP-1α mRNA levels increased at 3 h after ischemia. MCP-1, MIP-1α, and vascular endothelial growth factor protein levels were also increased markedly and were maximal on days 1, 0.5, and 1, respectively, after ischemia. In situ hybridization showed that MCP-1 and MIP-1α were localized in the hypoxic inner retina. Immunostaining demonstrated that the macrophages/microglia in the retina had morphological changes with enlarged processes, and some were closely associated with neovascular tufts at postnatal day 17. Coadministration of the neutralizing antibodies against MCP-1 and MIP-1α inhibited retinal neovascularization by 30%. Our data suggest that MCP-1 and MIP-1α are involved in the induction of retinal neovascularization and play a role in the inflammation induced by the ischemic retinopathy, possibly by modulating or attracting macrophages/microglia.

Original languageEnglish
Pages (from-to)137-144
Number of pages8
JournalJournal of Leukocyte Biology
Volume73
Issue number1
DOIs
Publication statusPublished - Jan 1 2003

All Science Journal Classification (ASJC) codes

  • Immunology and Allergy
  • Immunology
  • Cell Biology

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