Induction of calbindin‐D 28K gene and protein expression by physiological stimuli but not in calcium‐mediated degeneration in rat PC12 pheochromocytoma cells

FEBS Letters

Thomasset, Monique³  Copin, Marie-Christine¹  Biguet, Nicole Faucon²  Michel, Patrick P.¹  Agid, Yves¹  Vyas, Sheela¹ 

[1] INSERM U289, Hôpital de la Salpêtrière, 47 Boulevard de l'hôpital, Paris 75013, France;CNRS, 91198, Gif-Sur-Yvette France;INSERM U120, Hôpital Robert Debré, Paris 75019, France

关键词: Calbindin-D28K;    Calcium;    Degeneration;    Depolarization;    PC12 cell;    Trophic factor;   

DOI  :  10.1016/0014-5793(94)00821-3

学科分类：生物化学/生物物理

来源: John Wiley & Sons Ltd.

【 摘 要 】

To understand the role of calbindin-D 28K in neuronal degeneration, we examined its expression in differentiated PC12 cells in response to calcium intoxication, using the ionophore A23187 treatment, that results in cell degeneration and death. We first established that calbindin-D 28K is expressed in PC12 cells. The amounts of calbindin-D 28K mRNA and protein were increased by the differentiation factors, NGF and retinoic acid, but not by vitamin D₃. Calbindin-D 28K expression was also significantly up-regulated by stimuli (depolarization, low concentrations of Ca²⁺ ionophore A23187) which increase intracellular calcium levels within the physiological range. In contrast, the calbindin-D 28K mRNA and protein concentrations were not modulated by high concentrations of A23187, which resulted in cell degeneration and death. Experiments with the antisense oligonucleotides showed that, although the calbindin-D 28K protein levels were decreased significantly, the progression of degenerative changes induced by calcium via A23187, was not altered.

【 授权许可】

Unknown