Monocyte transplantation for neural and cardiovascular ischemia repair.
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.
Sanberg
Paul R
PR
Center of Excellence for Aging and Brain Repair, Department of Neurosurgery and Brain Repair, University of South Florida College of Medicine, Tampa, FL 33612, USA. psanberg@health.usf.edu
Park
Dong-Hyuk
DH
Kuzmin-Nichols
Nicole
N
Cruz
Eduardo
E
Hossne
Nelson Americo
NA
Buffolo
Enio
E
Willing
Alison E
AE
D000818:Animals; D002319:Cardiovascular System / Q000503:physiopathology; D005312:Fetal Blood / Q000166:cytology; D006801:Humans; D018836:Inflammation Mediators / Q000378:metabolism; D007511:Ischemia / Q000378:metabolism*; D008954:Models, Biological; D009000:Monocytes / Q000166:cytology / Q000378:metabolism* / Q000637:transplantation*; D018919:Neovascularization, Physiologic; D009420:Nervous System / Q000098:blood supply / Q000378:metabolism*
D018836:Inflammation Mediators