A novel role of hippocalcin in bFGF-induced neurite outgrowth of H19-7 cells

Doo Yi Oh, Hwan Cho Ju, Shin Young Park, Seok Kim Yong, Young Ju Yoon, Hee Yoon Shin, Chul Chung Kwang, Sung Lee Ki, Joong Soo Han

Research output: Contribution to journalArticle

15 Citations (Scopus)

Abstract

Hippocalcin is a Ca2+-binding protein that is expressed mainly in pyramidal nerve cells of the hippocampus. However, its functions and mechanism in the brain remain unclear. To elucidate the role of hippocalcin, we used a conditionally immortalized hippocampal cell line (H19-7) and showed that bFGF treatment increased the expression of hippocalcin during bFGF-induced neurite outgrowth of H19-7 cells. Overexpression of hippocalcin dramatically elongated neuntes and increased the expression of basic helix-loop-helix transcription factor, that is, NeuroD without bFGF stimulation. Treatment of the cells with hippocalcin siRNA completely blocked bFGF-induced neurite outgrowth and NeuroD expression. bFGF stimulation resulted in activation of phospholipase C-γ (PLC-γ) and an increased level of intracellular Ca2+. Hippocalcin expression by bFGF stimulation was fully blocked by both the PLC-γ inhibitor U73122 and BAPTA-AM, a chelator of intracellular Ca 2+, suggesting that hippocalcin expression by bFGF is dependent on PLC-γ and Ca2+. Moreover, both U73122 and BAPTA-AM completely blocked bFGF-induced neurite outgrowth and NeuroD expression. Taken together, these results suggest for the first time that bFGF induces hippocalcin expression in H19-7 cells through PLC-γ activation, which leads to neurite outgrowth.

Original languageEnglish
Pages (from-to)1557-1565
Number of pages9
JournalJournal of Neuroscience Research
Volume86
Issue number7
DOIs
Publication statusPublished - 2008 May 15

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Hippocalcin
Type C Phospholipases
Basic Helix-Loop-Helix Transcription Factors
Neuronal Outgrowth
Pyramidal Cells
Chelating Agents
Small Interfering RNA
Hippocampus
Carrier Proteins

All Science Journal Classification (ASJC) codes

  • Cellular and Molecular Neuroscience

Cite this

Oh, D. Y., Ju, H. C., Park, S. Y., Yong, S. K., Yoon, Y. J., Shin, H. Y., ... Han, J. S. (2008). A novel role of hippocalcin in bFGF-induced neurite outgrowth of H19-7 cells. Journal of Neuroscience Research, 86(7), 1557-1565. https://doi.org/10.1002/jnr.21602
Oh, Doo Yi ; Ju, Hwan Cho ; Park, Shin Young ; Yong, Seok Kim ; Yoon, Young Ju ; Shin, Hee Yoon ; Kwang, Chul Chung ; Ki, Sung Lee ; Han, Joong Soo. / A novel role of hippocalcin in bFGF-induced neurite outgrowth of H19-7 cells. In: Journal of Neuroscience Research. 2008 ; Vol. 86, No. 7. pp. 1557-1565.
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abstract = "Hippocalcin is a Ca2+-binding protein that is expressed mainly in pyramidal nerve cells of the hippocampus. However, its functions and mechanism in the brain remain unclear. To elucidate the role of hippocalcin, we used a conditionally immortalized hippocampal cell line (H19-7) and showed that bFGF treatment increased the expression of hippocalcin during bFGF-induced neurite outgrowth of H19-7 cells. Overexpression of hippocalcin dramatically elongated neuntes and increased the expression of basic helix-loop-helix transcription factor, that is, NeuroD without bFGF stimulation. Treatment of the cells with hippocalcin siRNA completely blocked bFGF-induced neurite outgrowth and NeuroD expression. bFGF stimulation resulted in activation of phospholipase C-γ (PLC-γ) and an increased level of intracellular Ca2+. Hippocalcin expression by bFGF stimulation was fully blocked by both the PLC-γ inhibitor U73122 and BAPTA-AM, a chelator of intracellular Ca 2+, suggesting that hippocalcin expression by bFGF is dependent on PLC-γ and Ca2+. Moreover, both U73122 and BAPTA-AM completely blocked bFGF-induced neurite outgrowth and NeuroD expression. Taken together, these results suggest for the first time that bFGF induces hippocalcin expression in H19-7 cells through PLC-γ activation, which leads to neurite outgrowth.",
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Oh, DY, Ju, HC, Park, SY, Yong, SK, Yoon, YJ, Shin, HY, Kwang, CC, Ki, SL & Han, JS 2008, 'A novel role of hippocalcin in bFGF-induced neurite outgrowth of H19-7 cells', Journal of Neuroscience Research, vol. 86, no. 7, pp. 1557-1565. https://doi.org/10.1002/jnr.21602

A novel role of hippocalcin in bFGF-induced neurite outgrowth of H19-7 cells. / Oh, Doo Yi; Ju, Hwan Cho; Park, Shin Young; Yong, Seok Kim; Yoon, Young Ju; Shin, Hee Yoon; Kwang, Chul Chung; Ki, Sung Lee; Han, Joong Soo.

In: Journal of Neuroscience Research, Vol. 86, No. 7, 15.05.2008, p. 1557-1565.

Research output: Contribution to journalArticle

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T1 - A novel role of hippocalcin in bFGF-induced neurite outgrowth of H19-7 cells

AU - Oh, Doo Yi

AU - Ju, Hwan Cho

AU - Park, Shin Young

AU - Yong, Seok Kim

AU - Yoon, Young Ju

AU - Shin, Hee Yoon

AU - Kwang, Chul Chung

AU - Ki, Sung Lee

AU - Han, Joong Soo

PY - 2008/5/15

Y1 - 2008/5/15

N2 - Hippocalcin is a Ca2+-binding protein that is expressed mainly in pyramidal nerve cells of the hippocampus. However, its functions and mechanism in the brain remain unclear. To elucidate the role of hippocalcin, we used a conditionally immortalized hippocampal cell line (H19-7) and showed that bFGF treatment increased the expression of hippocalcin during bFGF-induced neurite outgrowth of H19-7 cells. Overexpression of hippocalcin dramatically elongated neuntes and increased the expression of basic helix-loop-helix transcription factor, that is, NeuroD without bFGF stimulation. Treatment of the cells with hippocalcin siRNA completely blocked bFGF-induced neurite outgrowth and NeuroD expression. bFGF stimulation resulted in activation of phospholipase C-γ (PLC-γ) and an increased level of intracellular Ca2+. Hippocalcin expression by bFGF stimulation was fully blocked by both the PLC-γ inhibitor U73122 and BAPTA-AM, a chelator of intracellular Ca 2+, suggesting that hippocalcin expression by bFGF is dependent on PLC-γ and Ca2+. Moreover, both U73122 and BAPTA-AM completely blocked bFGF-induced neurite outgrowth and NeuroD expression. Taken together, these results suggest for the first time that bFGF induces hippocalcin expression in H19-7 cells through PLC-γ activation, which leads to neurite outgrowth.

AB - Hippocalcin is a Ca2+-binding protein that is expressed mainly in pyramidal nerve cells of the hippocampus. However, its functions and mechanism in the brain remain unclear. To elucidate the role of hippocalcin, we used a conditionally immortalized hippocampal cell line (H19-7) and showed that bFGF treatment increased the expression of hippocalcin during bFGF-induced neurite outgrowth of H19-7 cells. Overexpression of hippocalcin dramatically elongated neuntes and increased the expression of basic helix-loop-helix transcription factor, that is, NeuroD without bFGF stimulation. Treatment of the cells with hippocalcin siRNA completely blocked bFGF-induced neurite outgrowth and NeuroD expression. bFGF stimulation resulted in activation of phospholipase C-γ (PLC-γ) and an increased level of intracellular Ca2+. Hippocalcin expression by bFGF stimulation was fully blocked by both the PLC-γ inhibitor U73122 and BAPTA-AM, a chelator of intracellular Ca 2+, suggesting that hippocalcin expression by bFGF is dependent on PLC-γ and Ca2+. Moreover, both U73122 and BAPTA-AM completely blocked bFGF-induced neurite outgrowth and NeuroD expression. Taken together, these results suggest for the first time that bFGF induces hippocalcin expression in H19-7 cells through PLC-γ activation, which leads to neurite outgrowth.

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