Journal
CELLULAR IMMUNOLOGY
Volume 265, Issue 2, Pages 139-145Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.cellimm.2010.08.002
Keywords
Morphine; Angiogenesis; Innate immune system; HIF-1 alpha; Wound healing
Categories
Funding
- National Institutes of Health [R01 DA12104, R01 DA022935, K02 DA015349, P50 DA11806]
- Minneapolis Veterans Affairs Medical Center
- NATIONAL INSTITUTE ON DRUG ABUSE [R01DA022935, R01DA012104, P50DA011806, K02DA015349] Funding Source: NIH RePORTER
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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. (C) 2010 Elsevier Inc. All rights reserved.
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