PMID- 24666284
OWN - NLM
STAT- MEDLINE
DCOM- 20140929
LR  - 20211007
IS  - 1471-4159 (Electronic)
IS  - 0022-3042 (Linking)
VI  - 130
IP  - 4
DP  - 2014 Aug
TI  - HPC-1/syntaxin 1A and syntaxin 1B play distinct roles in neuronal survival.
PG  - 514-25
LID - 10.1111/jnc.12722 [doi]
AB  - Two types of syntaxin 1 isoforms, HPC-1/syntaxin 1A (STX1A) and syntaxin 1B 
      (STX1B), are thought to have similar functions in exocytosis of synaptic 
      vesicles. STX1A(-/-) mice which we generated previously develop normally, 
      possibly because of compensation by STX1B. We produced STX1B(-/-) mice using 
      targeted gene disruption and investigated their phenotypes. STX1B(-/-) mice were 
      born alive, but died before postnatal day 14, unlike STX1A(-/-) mice. 
      Morphologically, brain development in STX1B(-/-) mice was impaired. In 
      hippocampal neuronal culture, the cell viability of STX1B(-/-) neurons was lower 
      than that of WT or STX1A(-/-) neurons after 9 days. Interestingly, STX1B(-/-) 
      neurons survived on WT or STX1A(-/-) glial feeder layers as well as WT neurons. 
      However, STX1B(-/-) glial feeder layers were less effective at promoting survival 
      of STX1B(-/-) neurons. Conditioned medium from WT or STX1A(-/-) glial cells had a 
      similar effect on survival, but that from STX1B(-/-) did not promote survival. 
      Furthermore, brain-derived neurotrophic factor (BDNF) or neurotrophin-3 supported 
      survival of STX1B(-/-) neurons. BDNF localization in STX1B(-/-) glial cells was 
      disrupted, and BDNF secretion from STX1B(-/-) glial cells was impaired. These 
      results suggest that STX1A and STX1B may play distinct roles in supporting 
      neuronal survival by glia. Syntaxin 1A (STX1A) and syntaxin 1B (STX1B) are 
      thought to have similar functions as SNARE proteins. However, we found that STX1A 
      and STX1B play distinct roles in neuronal survival using STX1A(-/-) mice and 
      STX1B(-/-) mice. STX1B was important for neuronal survival, possibly by 
      regulating the secretion of neurotrophic factors, such as BDNF, from glial cells.
CI  - (c) 2014 International Society for Neurochemistry.
FAU - Kofuji, Takefumi
AU  - Kofuji T
AD  - Radioisotope Laboratory, Kyorin University School of Medicine, Mitaka, Tokyo, 
      Japan.
FAU - Fujiwara, Tomonori
AU  - Fujiwara T
FAU - Sanada, Masumi
AU  - Sanada M
FAU - Mishima, Tatsuya
AU  - Mishima T
FAU - Akagawa, Kimio
AU  - Akagawa K
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20140419
PL  - England
TA  - J Neurochem
JT  - Journal of neurochemistry
JID - 2985190R
RN  - 0 (Brain-Derived Neurotrophic Factor)
RN  - 0 (Munc18 Proteins)
RN  - 0 (Neurotrophin 3)
RN  - 0 (Syntaxin 1)
SB  - IM
CIN - J Neurochem. 2014 Aug;130(4):469-71. PMID: 24750130
MH  - Animals
MH  - Blotting, Western
MH  - Brain/growth & development
MH  - Brain-Derived Neurotrophic Factor/biosynthesis/pharmacology
MH  - Cell Survival/genetics/physiology
MH  - Immunoenzyme Techniques
MH  - Immunohistochemistry
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Mice, Knockout
MH  - Munc18 Proteins/metabolism
MH  - Neuroglia/physiology
MH  - Neurons/*physiology
MH  - Neurotrophin 3/biosynthesis/pharmacology
MH  - Real-Time Polymerase Chain Reaction
MH  - Syntaxin 1/genetics/*physiology
MH  - Transfection
OTO - NOTNLM
OT  - HPC-1/syntaxin 1A
OT  - glial cells
OT  - knockout mice
OT  - neuronal survival
OT  - syntaxin 1B
EDAT- 2014/03/29 06:00
MHDA- 2014/09/30 06:00
CRDT- 2014/03/27 06:00
PHST- 2013/12/20 00:00 [received]
PHST- 2014/03/23 00:00 [revised]
PHST- 2014/03/24 00:00 [accepted]
PHST- 2014/03/27 06:00 [entrez]
PHST- 2014/03/29 06:00 [pubmed]
PHST- 2014/09/30 06:00 [medline]
AID - 10.1111/jnc.12722 [doi]
PST - ppublish
SO  - J Neurochem. 2014 Aug;130(4):514-25. doi: 10.1111/jnc.12722. Epub 2014 Apr 19.