Research abstract

Article abstract


Nature Biotechnology 20, 1111 - 1117 (2002)
Published online: 15 October 2002 | doi:10.1038/nbt751

The injured brain interacts reciprocally with neural stem cells supported by scaffolds to reconstitute lost tissue

Kook In Park1,2, Yang D. Teng2,3 & Evan Y. Snyder2


Hypoxic-ischemic injury is a prototype for insults characterized by extensive tissue loss. Seeding neural stem cells (NSCs) onto a polymer scaffold that was subsequently implanted into the infarction cavities of mouse brains injured by hypoxia-ischemia allowed us to observe the multiple reciprocal interactions that spontaneously ensue between NSCs and the extensively damaged brain: parenchymal loss was dramatically reduced, an intricate meshwork of many highly arborized neurites of both host- and donor-derived neurons emerged, and some anatomical connections appeared to be reconstituted. The NSC–scaffold complex altered the trajectory and complexity of host cortical neurites. Reciprocally, donor-derived neurons were seemingly capable of directed, target-appropriate neurite outgrowth (extending axons to the opposite hemisphere) without specific external instruction, induction, or genetic manipulation of host brain or donor cells. These “biobridges” appeared to unveil or augment a constitutive reparative response by facilitating a series of reciprocal interactions between NSC and host, including promoting neuronal differentiation, enhancing the elaboration of neural processes, fostering the re-formation of cortical tissue, and promoting connectivity. Inflammation and scarring were also reduced, facilitating reconstitution.

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  1. Department of Pediatrics, Pharmacology, and Brain, Korea 21 Project for Medical Sciences, Yonsei University College of Medicine, Seoul, 120-752, Korea.
  2. Department of Neurology, Harvard Medical School, Boston, MA 02115, USA.
  3. Department of Neurosurgery, Harvard Medical School, Boston, MA 02115, USA.

Correspondence to: Evan Y. Snyder2 e-mail: esnyder1@caregroup.harvard.edu



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