Cellular and Molecular Neurobiology
Author: Estefania Chamorro Aguirre | Email: estefachamorro@gmail.com
Estefania Chamorro-Aguirre1°, Martina Garmendia1°,María Julia Pérez1°, Jorge Correale1°2°, Juana María Pasquini1°, Hugo Adamo1°
1° Departamento de Química Biológica e Instituto de Química y Fisicoquímica Biológicas “Dr Alejandro C. Paladini” (IQUIFIB), Facultad de Farmacia y Bioquímica. UBA-CONICET.
2° Departamento de Neurología FLENI.
Since 1994 our laboratory has maintained the hypothesis that apoTransferrin (aTf) is capable of accelerating the maturation of the oligodendroglial cell. The effect was demonstrated “in vivo” first and then “in vitro” and in different experimental models of demyelination and hypomyelination. However, this hypothesis was always questioned given that Tf is an iron transporter, and the question was whether it was an effect of Tf or the iron it transported.
In order to test our hypothesis, we decided to make use of previously described non-glycosylated Tf mutants by Mason et al., 2004. Tf mutant YF (Y95F/Y188F/Y426F/Y517F) is unable to bind iron either in the N-lobe or the C-lobe, while mutant KA (K206E/E534A) is unable to release iron. The oligodendroglial precursor cell line Oli-neu were transfected employed Lipofectamine 2000 either with the Tf wt or mutants. It was evaluated morphological changes using MBP (oligodendrocyte differentiation marker) by immunocytochemistry. The results show that, just as cells transfected with the WT do, the other two Tf mutans were able to produce maturation of the Oli-neu cells, undoubtedly indicating that it is Tf that accelerates their maturation and not iron. Since the morphology of the mature cells was different in the three situations, we investigated the causes of these differences.