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Review
. 2013 Apr;4(2):137-48.
doi: 10.1007/s12975-013-0254-5.

The potential for cell-based therapy in perinatal brain injuries

Andre W Phillips  1 , Michael V Johnston, Ali Fatemi
Affiliations
Review

The potential for cell-based therapy in perinatal brain injuries

Andre W Phillips et al. Transl Stroke Res. 2013 Apr.

Abstract

Perinatal brain injuries are a leading cause of cerebral palsy worldwide. The potential of stem cell therapy to prevent or reduce these impairments has been widely discussed within the medical and scientific communities and an increasing amount of research is being conducted in this field. Animal studies support the idea that a number of stem cells types, including cord blood and mesenchymal stem cells have a neuroprotective effect in neonatal hypoxia-ischemia. Both these cell types are readily available in a clinical setting. The mechanisms of action appear to be diverse, including immunomodulation, activation of endogenous stem cells, release of growth factors, and anti-apoptotic effects. Here, we review the different types of stem cells and progenitor cells that are potential candidates for therapeutic strategies in perinatal brain injuries, and summarize recent preclinical and clinical studies.

Keywords: Cerebral Palsy; Stem Cell; brain injury; hypoxia ischemia; neonate.

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Figures

Figure 1
Figure 1. Various types of Stem Cells
Adapted from: Mitalipov S, Wolf D. Adv Biochem Eng Biotechnol. 2009;114:185–99.
Figure 2
Figure 2. Fate of transplanted oligodendrocyte progenitors in a rat model of periventricular leukomalacia (adapted from Webber et al. Am J Pathol. 2009 December; 175(6): 2332–2342)
GFP-OPCs survive transplantation in a LPS induced rat PVL model for at least 8 weeks and commit to glial progeny. GFP cells were clearly in both gray and white matter at 8 weeks post-transplantation in lesioned animals (arrows) and were identified to express NG2 (arrowhead, red, B), a marker for OPCs, Olig2 (arrowhead, red, C), a marker for oligodendrocytes, and GFAP (arrowhead, red, D), a marker for astrocytes. Co-staining for the neuron specific marker, NeuN, was not observed at 8 weeks (E). The authors reported that the majority of GFP-positive cells co-labeled with Olig2 and NG2, while none was NeuN co-labeled (F).
Figure 3
Figure 3. Effect of intracerebral MSC treatment at 3 days after unilateral HI on lesion size and functional outcome (adapted from van Velthoven et al., Brain, Behavior, and Immunity Volume 24, Issue 3, March 2010, Pages 387–393)
MSC treatment reduced HI- induced Microtubule Associated Protein 2 (MAP2)+ area loss (A) and Myelin Basic Protein (MBP)+ area loss (B) expressed as ratio ipsi-/contralateral area. Furthermore, paw preference in the cylinder rearing test was determined as a measure of lateralizing motor deficits at 10 and 21 days after the insult and was significantly improved in cell treated animals (C). Data represent mean percentage area loss ± SEM or mean percentage difference between non-impaired and impaired forepaw initiation ± SEM. N = 10–12 animals per group. (●p < 0.05; ●●p < 0.01).
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