Monocyte transplantation for neural and cardiovascular ischemia repair

J Cell Mol Med. 2010 Mar;14(3):553-63. doi: 10.1111/j.1582-4934.2009.00903.x. Epub 2009 Sep 14.

Abstract

Neovascularization is an integral process of inflammatory reactions and subsequent repair cascades in tissue injury. Monocytes/macrophages play a key role in the inflammatory process including angiogenesis as well as the defence mechanisms by exerting microbicidal and immunomodulatory activity. Current studies have demonstrated that recruited monocytes/macrophages aid in regulating angiogenesis in ischemic tissue, tumours and chronic inflammation. In terms of neovascularization followed by tissue regeneration, monocytes/macrophages should be highly attractive for cell-based therapy compared to any other stem cells due to their considerable advantages: non-oncogenic, non-teratogenic, multiple secretary functions including pro-angiogenic and growth factors, straightforward cell harvesting procedure and non-existent ethical controversy. In addition to adult origins such as bone marrow or peripheral blood, umbilical cord blood (UCB) can be a potential source for autologous or allogeneic monocytes/macrophages. Especially, UCB monocytes should be considered as the first candidate owing to their feasibility, low immune rejection and multiple characteristic advantages such as their anti-inflammatory properties by virtue of their unique immune and inflammatory immaturity, and their pro-angiogenic ability. In this review, we present general characteristics and potential of monocytes/macrophages for cell-based therapy, especially focusing on neovascularization and UCB-derived monocytes.

Publication types

  • Review

MeSH terms

  • Animals
  • Cardiovascular System / physiopathology
  • Fetal Blood / cytology
  • Humans
  • Inflammation Mediators / metabolism
  • Ischemia / metabolism*
  • Models, Biological
  • Monocytes / cytology
  • Monocytes / metabolism*
  • Monocytes / transplantation*
  • Neovascularization, Physiologic
  • Nervous System / blood supply
  • Nervous System / metabolism*

Substances

  • Inflammation Mediators