Identification of a potent neurotrophic substance for ciliary ganglionic neurons in fetal calf serum as insulin-like growth factor II

• Verfasst von: Motoike, Toshiyuki [VerfasserIn]
• Verfasst von: Unsicker, Klaus [VerfasserIn]
• Titel: Identification of a potent neurotrophic substance for ciliary ganglionic neurons in fetal calf serum as insulin-like growth factor II
• Verf.angabe: Toshiyuki Motoike and Klaus Unsicker
• Umfang: 11 S.
• Fussnoten: Gesehen am 24.11.2016
• Titel Quelle: Enthalten in: Journal of neuroscience research
• Jahr Quelle: 1999
• Band/Heft Quelle: 56(1999), 4, S. 386-396
• ISSN Quelle: 1097-4547
• DOI: doi:10.1002/(SICI)1097-4547(19990515)56:4<386¬AID-JNR6>3.0.CO;2-D
• Datenträger: Online-Ressource
• Sprache: eng
• K10plus-PPN: 1550111043

Abstract

When fetal calf serum (FCS) alone is used as a trophic support for cultured chicken parasympathetic ciliary ganglionic (cCG) neurons, it does not show any survival-promoting effects on these neurons. When FCS is applied to heparin-affinity chromatography, however, potent survival-promoting activity is obtained in the fraction eluted with 0.5 M NaCl. Using cCG neurons as a bioassay system, this neurotrophic activity was purified by a combination of heparin-affinity chromatography, gel filtration chromatography, and Sep-Pak C18 cartridge. The 40-50-kDa fractions from the gel filtration column with strong survival-promoting activity were shown to contain insulin-like growth factor II (IGF-II) by immunoblot analysis. By acidification, the survival-promoting activity and IGF-II were translocated together from the 40-50-kDa to the 7-10-kDa fractions, and the survival-promoting activity in the 7-10-kDa fractions was blocked by an anti-IGF-II neutralizing monoclonal antibody. These results indicate that the neurotrophic substance in 0.5 M NaCl-eluate from heparin-affinity chromatography is IGF-II and that mechanisms may exist in vivo for the activation of latent IGF-II, whose biological effects may be blocked by its specific binding proteins. J. Neurosci. Res. 56:386-396, 1999. © 1999 Wiley-Liss, Inc.