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The Journal of Neuroscience, November 15, 1999, 19(22):9964-9974

Galectin-1 Regulates Initial Axonal Growth in Peripheral Nerves after Axotomy

Hidenori Horie¹, Yoshimasa Inagaki⁴, Yoshiaki Sohma⁴, Risa Nozawa⁴, Katsuya Okawa⁵, Mitsuhiro Hasegawa⁶, Naoki Muramatsu⁶, Hitoshi Kawano⁷, Masao Horie⁷, Hiromichi Koyama³, Ikuko Sakai¹, Kaori Takeshita¹, Yuki Kowada¹, Masahiko Takano², and Toshihiko Kadoya⁴

Departments of ¹ Physiology and ² Ophthalmology, School of Medicine, and ³ College of Nursing, Yokohama City University, Kanazawa-ku, Yokohama 236-0004, Japan, ⁴ Pharmaceutical Research Laboratory, Kirin Brewery Co., Ltd., Takasaki 370-1295, Japan, ⁵ Central Laboratories for Key Technology, Kirin Brewery Co., Ltd., Kanazawa-ku, Yokohama 236-0004, Japan, ⁶ Department of Neurosurgery, Kanazawa University School of Medicine, Kanazawa 920-0934, Japan, and ⁷ Department of Anatomy and Embryology, Tokyo Metropolitan Institute of Neuroscience, Fuchu, Tokyo 183-8526, Japan

The signals that prompt the axons to send out processes in peripheral nerves after axotomy are not well understood. Here, we report that galectin-1 can play an important role in this initial stage. We developed an in vitro nerve regeneration model that allows us to monitor the initial axon and support cell outgrowth from the proximal nerve stump, which is comparable to the initial stages of nerve repair. We isolated a factor secreted from COS1 cells that enhanced axonal regeneration, and we identified the factor as galectin-1. Recombinant human galectin-1 (rhGAL-1) showed the same activity at low concentrations (50 pg/ml) that are two orders of magnitude lower than those of lectin activity. A similarly low concentration was also effective in in vivo experiments of axonal regeneration with migrating reactive Schwann cells to a grafted silicone tube after transection of adult rat peripheral nerve. Moreover, the application of functional anti-rhGAL-1 antibody strongly inhibited the regeneration in vivo as well as in vitro. The same effect of rhGAL-1 was confirmed in crush/freeze experiments of the adult mouse sciatic nerve. Because galectin-1 is expressed in the regenerating sciatic nerves as well as in both sensory neurons and motor neurons, we suggest that galectin-1 may regulate initial repair after axotomy. This high activity of the factor applied under nonreducing conditions suggests that galectin-1 may work as a cytokine, not as a lectin.

Key words: galectin-1; growth factor; regeneration; nerve transection; nerve crush; peripheral nerve; COS1 cell; organ culture; dorsal root ganglion; axotomy

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Copyright © 1999 Society for Neuroscience  0270-6474/99/19229964-11$05.00/0

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