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Review
. 2015 Aug;46(8):2354-63.
doi: 10.1161/STROKEAHA.114.007803. Epub 2015 Jun 23.

Stem Cell-Based Tissue Replacement After Stroke: Factual Necessity or Notorious Fiction?

Miroslaw Janowski  1 , Daniel-Christoph Wagner  1 , Johannes Boltze  2
Affiliations
Review

Stem Cell-Based Tissue Replacement After Stroke: Factual Necessity or Notorious Fiction?

Miroslaw Janowski et al. Stroke. 2015 Aug.
No abstract available

Keywords: brain; nerve regeneration; neurons; stem cell transplantation; stroke; tissue engineering; tissue-type plasminogen activator.

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Figures

Figure 1
Figure 1. Post-stroke tissue restoration in theory and practice
(A) In theory, tissue restoration strategies will have to target all three major cerebral cell populations: neurons, astro- and oligodendrocytes. Replacement of each individual component may come with different challenges. (B) In a recent study, MGE-grafted cells enhanced synaptophysin expression, which was quantified in the contralateral and ipsilateral sides (insets in brain slice scheme). Data are expressed as mean ± SEM. *p<0.05 versus vehicle (C) Representative current clamp trace of an action potential from an MGE neuron, implanted into the dorsal striatum of a stroked rat, elicited in response to a 400 pA current injection (left diagram). Sample trace of spontaneous excitatory postsynaptic currents (sEPSCs) in the MGE neuron held at −70 mV (native resting membrane potential for this cell was −56 mV; right diagram). (B) and (C) modified from by Daadi et al. (Cell Transplant. 2009;18:815–826. doi: 10.3727/096368909X470829; courtesy of Cognizant Communication Corporation, Putnam Valley, NY 10579, USA)
Figure 2
Figure 2. Structural support of stem cell grafts
Overview on different cerebral tissue restoration strategies using pluripotent stem cell populations with or without structural support. Future, “true” restorative strategies will most likely have to rely on scaffold support.
Figure 3
Figure 3. Pathophysiological aspects following ischemic stroke
A plethora of stroke sequelae contribute to immediate and delayed cell loss and impaired regeneration. Transplanted cells have been shown to affect relevant pathophysiological mechanisms, but successful treatment seems to be highly dependent on the time point of transplantation. When administered in the acute phase of stroke, cells can attenuate primary neural cell death, detrimental neuroinflammation and promote vascular repair and neovascularization. These early effects were frequently observed together with low or absent cell survival and integration, or even rely on cell scavenging. By contrast, the modulation of factors determining stroke outcome in the chronic phase seems to require prolonged presence of transplanted cells. Therapeutically relevant brain repair and attenuation of chronic inflammation demands the secretion of sufficient amounts of trophic factors and continuous manipulation of perivascular spaces.
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