Chronic morphine treatment inhibits LPS-induced angiogenesis: Implications in wound healing

Josephine L. Martin, Richard Charboneau, Roderick A. Barke, Sabita Roy

Research output: Contribution to journalArticle

44 Scopus citations


Delayed wound healing is a chronic problem in opioid drug abusers. We investigated the role chronic morphine plays on later stages of wound healing events using an angiogenesis model. Our results show that morphine treatment resulted in a significant decrease in inflammation induced angiogenesis. To delineate the mechanisms involved we investigate the role of hypoxia inducible factor 1 alpha (HIF-1 alpha), a potent inducer of angiogenic growth factor. Morphine treatment resulted in a significant decrease in the expression and nuclear translocation of HIF-1 alpha with a concurrent suppression in vascular endothelial growth factor (VEGF) synthesis. Cells of the innate immune system play a dominant role in the angiogenic process. Morphine treatment inhibited early recruitment of both neutrophils and monocytes towards an inflammatory signal with a significant decrease in the monocyte chemoattractant MCP-1. Taken together, our studies show that morphine regulates the wound repair process on multiple levels. Morphine acts both directly and indirectly in suppressing angiogenesis.

Original languageEnglish (US)
Pages (from-to)139-145
Number of pages7
JournalCellular Immunology
Issue number2
StatePublished - Sep 15 2010



  • Angiogenesis
  • HIF-1 alpha
  • Innate immune system
  • Morphine
  • Wound healing

ASJC Scopus subject areas

  • Immunology

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