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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 
 
 
 
 

Regulation of the ferritin H subunit by vitamin B12 (cobalamin) in rat spinal cord.

Cobalamin-deficient (Cbl-D) central neuropathy is a pure myelinolytic disease, in which gliosis is also observed. Iron is abundant in the mammalian central nervous system, where it is required for various essential functions including myelinogenesis. It is predominantly located in the white matter and oligodendrocytes, which also actively synthesize the major iron proteins (e.g., ferritin, transferrin). We investigated the expression of the main proteins of iron metabolism in the spinal cord (SC) of totally gastrectomized Cbl-D rats 2 months after surgery (i.e., when the Cbl-D status has become severe). There were no significant changes in iron content, the activity of iron regulatory proteins, or the expression of transferrin or its receptor in the SC. We observed a significant decrease in the levels of both H and L ferritin subunits, with a more marked reduction in the latter. Post-operative cobalamin replacement therapy normalized only the H-ferritin subunits, and only in the SC. Our results therefore suggest that permanent cobalamin deficiency affects iron metabolism in the rat SC preferentially from a functional point of view, because H-ferritin is known to be involved in the uptake and release of iron.[1]

References

  1. Regulation of the ferritin H subunit by vitamin B12 (cobalamin) in rat spinal cord. Cairo, G., Ronchi, R., Buccellato, F.R., Veber, D., Santambrogio, P., Scalabrino, G. J. Neurosci. Res. (2002) [Pubmed]
 
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