Effects of nitric oxide on stem cell therapy

被引:20
作者
Wang, Wuchen [1 ]
Lee, Yugyung [2 ]
Lee, Chi H. [1 ]
机构
[1] Univ Missouri, Sch Pharm, Kansas City, MO 64108 USA
[2] Univ Missouri, Sch Comp & Engn, Kansas City, MO 64108 USA
关键词
Nitric oxide; Stem cell therapy; Novel platforms for NO delivery; SKELETAL-MUSCLE REGENERATION; ENDOTHELIAL GROWTH-FACTOR; MEDIATED IMMUNOSUPPRESSION; OXIDATIVE STRESS; PROGENITOR CELLS; BV2; MICROGLIA; MOUSE MODEL; NO-DONOR; DIFFERENTIATION; SYNTHASE;
D O I
10.1016/j.biotechadv.2015.09.004
中图分类号
Q81 [生物工程学(生物技术)]; Q93 [微生物学];
学科分类号
071005 ; 0836 ; 090102 ; 100705 ;
摘要
The use of stem cells as a research tool and a therapeutic vehicle has demonstrated their great potential in the treatment of various diseases. With unveiling of nitric oxide synthase (NOS) universally present at various levels in nearly all types of body tissues, the potential therapeutic implication of nitric oxide (NO) has been magnified, and thus scientists have explored new treatment strategies involved with stem cells and NO against various diseases. As the functionality of NO encompasses cardiovascular, neuronal and immune systems, NO is involved in stem cell differentiation, epigenetic regulation and immune suppression. Stem cells trigger cellular responses to external signals on the basis of both NO specific pathways and concerted action with endogenous compounds including stem cell regulators. As potency and interaction of NO with stem cells generally depend on the concentrations of NO and the presence of the cofactors at the active site, the suitable carriers for NO delivery is integral for exerting maximal efficacy of stem cells. The innovative utilization of NO functionality and involved mechanisms would invariably alter the paradigm of therapeutic application of stem cells. Future prospects in NO-involved stem cell research which promises to enhance drug discovery efforts by opening new era to improve drug efficacy, reduce drug toxicity and understand disease mechanisms and pathways, were also addressed. Published by Elsevier Inc.
引用
收藏
页码:1685 / 1696
页数:12
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