[Abstract Title]. - Society for Neuroscience

was also blocked by the TPEN-treatment. Therefore, we propose that intracellular zinc
accumulation causes the event of programmed cell death in the developing brain. By contrast,
although TPEN chelates other metal ion (e.g. iron or copper) as well as zinc, their involvements
in the developmental apoptosis were ruled out because the intracellular accumulation of labile
iron or copper ion was not found by Perl‟s stain or Phen Green SK (PGSK) fluorescent dye.
Disclosures: J. Lee, None; E. Cho, None; H. Jeong, None; J. Koh, None.
Poster
232. Developmental Cell Death: Biological Effects
Time: Sunday, November 16, 2008, 1:00 pm - 5:00 pm
Program#/Poster#: 232.23/B63
Topic: A.06.c. Developmental cell death: Other trophic factors
Support: Istituto Pasteur Fondazione Cenci Bolognetti, Sapienza Univ Rome
Ateneo 2006-2007
Title: De novo transcription of the Thg-1pit gene and translocation of the protein product to the
nuclear matrix landmark the onset of apoptosis in cerebellum granule neurons of the mouse
Authors: S. CANTERINI 1 , A. BOSCO 1 , V. DE MATTEIS 1 , F. MANGIA 1,2 , *M.
FIORENZA 1,2 ;
1 Sapienza Univ. Rome, Rome, Italy; 2 Neurobio. Res. Ctr. "D. Bovet", Rome, Italy
Abstract: Thg-1pit belongs to the transforming growth factor (TGF)-beta-stimulated clone 22
domain (TSC22D) gene family, coding for proteins widely expressed in developing and adult
mouse tissues (Kester et al., 2000; Treisman et al., 1995; Dohrmann et al., 2000).
Proteins encoded by these genes act as transcriptional regulators and influence a number of
biological processes, including cell proliferation, apoptosis and stress response. Based on our
previous findings on Thg-1pit expression in developing and adult cerebellum granule neurons
(CGN) (Canterini et al., 2005), we have exploited primary CGN in vitro cultures to gain insight
on the function of this gene. CGN cultures have widely been used to investigate the anti/proapoptotic
effect exerted on these cells by growth factors/cytokines as Insulin-like Growth Factor
1 (IGF1) and Transforming Growth Factor-β (TGF-β) (rev. by Vaudry et al., 2003), as well as
the dependence of CGN survival/apoptosis on membrane electrical activity (D‟Mello et al.,
1993). In fact, lowering the level of K + in the culture medium ([K + ]ext) from 25 mM to 5 mM
triggers CGN apoptosis, while TGF-β apparently has opposite roles, by promoting apoptosis
when administered with 5 mM [K + ]ext, and cell survival in the presence of 25 mM [K + ]ext (de