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Valproic Acid Promotes Neurite Outgrowth in PC12 Cells independent from Regulation of the Survival of Motoneuron Protein
Author(s) -
Bergeijk Jeroen,
Haastert Kirsten,
Grothe Claudia,
Claus Peter
Publication year - 2006
Publication title -
chemical biology and drug design
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.59
H-Index - 77
eISSN - 1747-0285
pISSN - 1747-0277
DOI - 10.1111/j.1747-0285.2006.00369.x
Subject(s) - neurite , smn1 , spinal muscular atrophy , sma* , valproic acid , downregulation and upregulation , microbiology and biotechnology , histone deacetylase , biology , phenotype , chemistry , cancer research , gene , neuroscience , biochemistry , histone , in vitro , epilepsy , mathematics , combinatorics
Spinal muscular atrophy (SMA) is a neurodegenerative disorder of motoneurons. The disease is caused by deletions or mutations of the survival of motoneuron gene 1 ( SMN1 ). The amount of protein expressed from the second gene, SMN2 , correlated with the severity of the clinical phenotype. The histone deacetylase inhibitor valproic acid (VPA) has been shown to increase the total cellular amount of functional SMN protein and is therefore considered as a drug candidate for treatment of SMA. In this study, we analyzed the effects of VPA in PC12 cells, a model system for neuronal differentiation, with regard to neurite outgrowth and SMN expression. VPA promoted neurite outgrowth in PC12 cells. However, this effect did not correlate with upregulation of SMN protein levels, suggesting a SMN‐independent mechanism for VPA regulation of neurite outgrowth.