TY - JOUR
T1 - 1α, 25 dihydroxyvitamin D3-dependent up-regulation of calcium-binding proteins in motoneuron cells
AU - Alexianu, Maria E.
AU - Robbins, Elaine
AU - Carswell, Susan
AU - Appel, Stanley H.
N1 - Copyright:
Copyright 2018 Elsevier B.V., All rights reserved.
PY - 1998/1/1
Y1 - 1998/1/1
N2 - 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.
AB - 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.
KW - 1,25 dihydroxyvitamin D
KW - Amyotrophic lateral sclerosis
KW - Calcium binding proteins
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U2 - 10.1002/(SICI)1097-4547(19980101)51:1<58::AID-JNR6>3.0.CO;2-K
DO - 10.1002/(SICI)1097-4547(19980101)51:1<58::AID-JNR6>3.0.CO;2-K
M3 - Article
C2 - 9452309
AN - SCOPUS:0031594331
SN - 0360-4012
VL - 51
SP - 58
EP - 66
JO - Journal of Neuroscience Research
JF - Journal of Neuroscience Research
IS - 1
ER -