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Author Kikuchi, Keietsu ♦ Shiota, Jun ♦ Yamada, Tetsuya ♦ Ishikawa, Mitsuru ♦ Ihara, Daisuke ♦ Fukuchi, Mamoru ♦ Tsuda, Masaaki ♦ Tabuchi, Akiko
Source United States Department of Energy Office of Scientific and Technical Information
Content type Text
Language English
Subject Keyword APPLIED LIFE SCIENCES ♦ ACTIN ♦ BROMIDES ♦ DENDRITES ♦ ELONGATION ♦ LEUKEMIA ♦ MICROTUBULES ♦ MORPHOLOGY ♦ NERVE CELLS ♦ PHOSPHATASES ♦ RATS ♦ TIME DEPENDENCE ♦ TRANSCRIPTION ♦ TRANSCRIPTION FACTORS ♦ VERTEBRAE
Abstract CCG-1423, a chemical inhibitor of Rho signaling, blocks serum response factor (SRF)/megakaryoblastic leukemia 1 (MKL1)-mediated gene expression by inhibiting the nuclear accumulation of MKL1. Several studies have suggested that CCG-1423 interacts not only with MKL1, which has a critical role in the regulation of neuronal morphology, but also with phosphatase and actin regulator 1 (Phactr1), which is localized at synapses. However, the effect of CCG-1423 on neuronal cells, especially on neuronal morphology, remains to be determined. In this study, we focused on the effect of CCG-1423 on axonal elongation, dendritic length, dendritic complexity and dendritic spine morphology. Incubation of cortical neuron cultures with up to 10 μM CCG-1423 for 72 h did not significantly affect cell viability. CCG-1423 inhibited axonal elongation and blocked the increase of dendritic length and complexity, but did not affect dendritic spine morphology. Here, we demonstrated for the first time that CCG-1423 affects neurite elongation, except for dendritic spines, without affecting neuronal cell viability. This study provides a better understanding of the effects of CCG-1423 on neurons, which may be useful for the assessment of the potential clinical application of CCG-1423 and its derivatives. - Highlights: • CCG-1423 does not affect neuronal cell viability. • CCG-1423 inhibits axonal elongation in rat cortical neurons. • CCG-1423 decreases dendritic complexity in a time-dependent manner.
ISSN 0006291X
Educational Use Research
Learning Resource Type Article
Publisher Date 2017-10-21
Publisher Place United States
Journal Biochemical and Biophysical Research Communications
Volume Number 492
Issue Number 3


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