1α, 25 dihydroxyvitamin D3-dependent up-regulation of calcium-binding proteins in motoneuron cells

Maria E. Alexianu, Elaine Robbins, Susan Carswell, Stanley H. Appel

Research output: Contribution to journalArticle

58 Scopus citations

Abstract

Our standing of selective neuronal vulnerability as well as etiopathogenesis of sporadic neurodegerative diseases is extremely limited. In ALS, altered calcium homeostasis appears to contribute significantly to selective neuronal injury. Further in ALS, the absence of calcium binding proteins (calbindin-D(28K), parvalbumin, and calretinin) correlates with selective vulnerability and cell loss. In motoneuron cell culture models an ALS IgG-triggered and calcium-mediated destruction can be reversed by increased expression of calbindin-D(28K) following retroviral infection with calbindin-D(28K) cDNA. To increase calcium binding protein expression in motoneurons in vitro and in vivo, we have employed vitamin D3. Forty-eight hr treatment of diffentiated VSC 4.1 cells with 0.1-30 nM 1,25 dihydroxyvitamin D3 induced a two-fold increase in the immunoreactivity for calbindin-D(28K) and parvalbumin. Injection of 80-120 ng, 1,25 dihydroxyvitamin D3 in the cerebral ventricles of adults rats also induced positive immunoreactivity in adult stage. These data suggest that analogs of 1,25 dihydroxyvitamin D3 may be useful tools in enhancing the expression of calcium binding proteins in motor system and may have possible therapeutic value in neurodegenerative disease.

Original languageEnglish (US)
Pages (from-to)58-66
Number of pages9
JournalJournal of Neuroscience Research
Volume51
Issue number1
DOIs
StatePublished - Jan 1 1998

Keywords

  • 1,25 dihydroxyvitamin D
  • Amyotrophic lateral sclerosis
  • Calcium binding proteins

ASJC Scopus subject areas

  • Neuroscience(all)

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