PMID- 18264755
OWN - NLM
STAT- MEDLINE
DCOM- 20081210
LR  - 20211203
IS  - 0272-4340 (Print)
IS  - 0272-4340 (Linking)
VI  - 28
IP  - 6
DP  - 2008 Sep
TI  - Endoplasmic reticulum stress upregulates the chondroitin sulfate level which thus 
      prevents neurite extension in C6 glioma cells and primary cultured astrocytes.
PG  - 857-66
LID - 10.1007/s10571-008-9262-5 [doi]
AB  - Chondroitin sulfate (CS), which is known to be a neurite-preventing molecule, is 
      a major component of the extracellular matrix (ECM) in the central nervous system 
      (CNS). The CS expression is upregulated around damaged areas. Endoplasmic 
      reticulum (ER) stress causes neuronal cell death in numerous neurodegenerative 
      diseases. However, the effects of ER stress on glial cells remain to be 
      clarified. The present study examined whether direct ER stress to glial cells can 
      upregulate CS expression in C6 glioma cells and primary cultured mouse 
      astrocytes, and also whether the expression of CS prevents neurite extension. ER 
      stressors tunicamycin (TM) and thapsigargin (TG) significantly increased CS 
      expression in both C6 cells and primary cultured astrocytes, while NO donor 
      sodium nitroprusside (SNP) did not significantly alter the CS expression. The 
      dosage of TM and TG treatment used in this study did not significantly induce 
      cell death but upregulated the ER chaperone molecule Grp78 in C6 glioma cells and 
      primary astrocytes. The ECM of glial cells exposed to ER stress prevented neurite 
      extension in primary cultured mouse cortical neurons, and chondroitinase ABC 
      (ChABC) treatment diminished the inhibitory effect on neurite extension. These 
      findings suggest that direct ER stress to glial cells increases the CS 
      expression, which thus prevents neurite extension.
FAU - Natori, Takamitsu
AU  - Natori T
AD  - Department of Epigenetic Medicine, Interdisciplinary Graduate School of Medicine 
      and Engineering, University of Yamanashi, Yamanashi, 409-3898, Japan.
FAU - Nagai, Kaoru
AU  - Nagai K
LA  - eng
PT  - Journal Article
DEP - 20080209
PL  - United States
TA  - Cell Mol Neurobiol
JT  - Cellular and molecular neurobiology
JID - 8200709
RN  - 0 (Endoplasmic Reticulum Chaperone BiP)
RN  - 0 (Hspa5 protein, mouse)
RN  - 0 (Nitric Oxide Donors)
RN  - 11089-65-9 (Tunicamycin)
RN  - 169D1260KM (Nitroprusside)
RN  - 67526-95-8 (Thapsigargin)
RN  - 9007-28-7 (Chondroitin Sulfates)
SB  - IM
MH  - Animals
MH  - Astrocytes/metabolism/*ultrastructure
MH  - Cell Line, Tumor
MH  - Cell Survival
MH  - Cells, Cultured
MH  - Chondroitin Sulfates/*biosynthesis
MH  - Endoplasmic Reticulum/*metabolism
MH  - Endoplasmic Reticulum Chaperone BiP
MH  - Glioma
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Neurites/*physiology
MH  - Neurons/ultrastructure
MH  - Nitric Oxide Donors/pharmacology
MH  - Nitroprusside/pharmacology
MH  - Rats
MH  - Thapsigargin/pharmacology
MH  - Tunicamycin/pharmacology
EDAT- 2008/02/12 09:00
MHDA- 2008/12/17 09:00
CRDT- 2008/02/12 09:00
PHST- 2007/10/22 00:00 [received]
PHST- 2008/01/18 00:00 [accepted]
PHST- 2008/02/12 09:00 [pubmed]
PHST- 2008/12/17 09:00 [medline]
PHST- 2008/02/12 09:00 [entrez]
AID - 10.1007/s10571-008-9262-5 [doi]
PST - ppublish
SO  - Cell Mol Neurobiol. 2008 Sep;28(6):857-66. doi: 10.1007/s10571-008-9262-5. Epub 
      2008 Feb 9.