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Umbilical cord blood mesenchymal stem cells co‐modified by TERT and BDNF: A novel neuroprotective therapy for neonatal hypoxic‐ischemic brain damage
Author(s) -
Zhao Fengyan,
Qu Yi,
Liu Haiting,
Du Baowen,
Mu Dezhi
Publication year - 2014
Publication title -
international journal of developmental neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.761
H-Index - 88
eISSN - 1873-474X
pISSN - 0736-5748
DOI - 10.1016/j.ijdevneu.2014.06.014
Subject(s) - mesenchymal stem cell , neuroprotection , medicine , neurotrophic factors , umbilical cord , brain damage , stem cell , stem cell therapy , brain derived neurotrophic factor , neural stem cell , cord blood , neurotrophin , immunology , neuroscience , bioinformatics , cancer research , pathology , pharmacology , biology , microbiology and biotechnology , receptor
Hypoxic‐ischemic brain damage (HIBD), a leading cause of perinatal disability and death, has limited therapeutic options. Stem cell therapy has been demonstrated as a potential novel therapy for neurological disorders. Compared with other types of stem cells, umbilical cord blood mesenchymal stem cells (UCB‐MSCs) have several unique characteristics, such as a higher rate of cell proliferation and clonality. However, the limited life span of UCB‐MSCs hinders their clinical application. Therefore, efforts are urgently needed to circumvent this disadvantage. Telomerase reverse transcriptase (TERT), which promotes cell proliferation and survival, plays a protective role in hypoxic‐ischemic (HI) brain injury. Thus, it is reasonable to propose that UCB‐MSCs modified by exogenous TERT expression might have a longer lifespan and increased viability. Moreover, brain‐derived neurotrophic factor (BDNF), a neurotrophin that regulates development, regeneration, survival and maintenance of neurons, facilitates post‐injury recovery when administered by infusion or virus‐mediated delivery. Therefore, TERT‐ and BDNF‐modified UCB‐MSCs may have a longer lifespan and also maintain neural differentiation, thus promoting the recovery of neurological function following hypoxic‐ischemic brain damage (HIBD) and thereby representing a new effective strategy for HIBD in neonates.