Neuroscience 2003 Abstract
| Presentation Number: | 677.18 |
|---|---|
| Abstract Title: | Sigma-1 receptors regulate cellular differentiation and proliferation in response to growth factors in PC12 cells. |
| Authors: |
Takebayashi, M.*1
; Hayashi, T.1
; Su, T. P.1
1Cell. Neurobiol Res. Br., NIDA/NIH/DHHS, Baltimore, MD |
| Primary Theme and Topics |
Development - Trophic Factors and Developmental Cell Death -- Neurotrophins: receptors and signaling mechanisms |
| Secondary Theme and Topics | Development<br />- Axonal and Dendritic Development<br />-- Axon growth and guidance: receptors and signaling mechanisms |
| Session: |
677. Trophic Factor Receptors & Signaling II Poster |
| Presentation Time: | Tuesday, November 11, 2003 2:00 PM-3:00 PM |
| Location: | Morial Convention Center - Hall F-I, Board # B65 |
| Keywords: | ANTIDEPRESSANT, EGF, AKT, ERK |
Sigma-1 receptors (Sig-1R) are unique endoplasmic reticulum proteins that bind (+)benzomorphans, neurosteroids, and certain psychotropic drugs such as antidepressants. We previously reported that PC12 cells stably overexpressing Sig-1R (MT 40 cells) exhibit a potentiation of the nerve growth factor (NGF)-induced neurite growth (JPET, 303:1227, 2002). Epidermal growth factor (EGF), which is known to lead to proliferation but not neurite outgrowth, however, can induce neurite outgrowth in MT 40 cells (SFN 2002). Here, we further characterized MT40 cells to examine the potential consequences of Sig-1R overexpression, especially, on the proliferation and associated-intracellular signalings. In the presence of EGF, wild type cells proliferated at least one-fold as much when compared to MT40 cells. In MT40cells, EGF-induced Akt phosphorylation, which is important in proliferation, was decreased, whereas EGF-induced phosphorylation of extracellular signaling-regulated protein kinase (ERK), critical for neurite outgrowth, was increased and prolonged. Although the exact relation to proliferation or differentiation is unclear, EGF receptor phosphorylation caused by EGF was enhanced in MT40 cells. Our data indicate that stable overexpression of Sig-1R shifts the action of EGF from favoring the proliferation to differentiation.
Supported by IRP/NIDA/NIH
Sample Citation:
[Authors]. [Abstract Title]. Program No. XXX.XX. 2003 Neuroscience Meeting Planner. New Orleans, LA: Society for Neuroscience, 2003. Online.
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