PMID- 26950456
OWN - NLM
STAT- MEDLINE
DCOM- 20161213
LR  - 20161230
IS  - 1165-158X (Electronic)
IS  - 0145-5680 (Linking)
VI  - 62
IP  - 2
DP  - 2016 Feb 29
TI  - Effects of c-Jun N-terminal kinase on Activin A/Smads signaling in PC12 cell 
      suffered from oxygen-glucose deprivation.
PG  - 81-6
AB  - Activin A (Act A), a member of transforming growth factor-beta (TGF-beta) superfamily, 
      is an early gene in response to cerebral ischemia. Growing evidences confirm the 
      neuroprotective effect of Act A in ischemic injury through Act A/Smads signal 
      activation. In this process, regulation networks are involved in modulating the 
      outcomes of Smads signaling. Among these regulators, crosstalk between c-Jun 
      N-terminal kinase (JNK) and Smads signaling has been found in the TGF-beta induced 
      epithelial-mesenchymal transition. However, in neural ischemia, the speculative 
      regulation between JNK and Act A/Smads signaling pathways has not been clarified. 
      To explore this issue, an Oxygen Glucose Deprivation (OGD) model was introduced 
      to nerve-like PC12 cells. We found that JNK signal activation occurred at the 
      early time of OGD injury (1 h). Act A administration suppressed JNK 
      phosphorylation. In addition, JNK inhibition could elevate the strength of Smads 
      signaling and attenuate neural apoptosis after OGD injury. Our results indicated 
      a negative regulation effect of JNK on Smads signaling in ischemic injury. Taken 
      together, JNK, as a critical site for neural apoptosis and negative regulator for 
      Act A/Smads signaling, was presumed to be a molecular therapeutic target for 
      ischemia.
FAU - Wang, J Q
AU  - Wang JQ
AD  - Jilin University Department of Neurology, China-Japan Union Hospital Changchun 
      China.
FAU - Xu, Z H
AU  - Xu ZH
AD  - Jilin University Clinical Medicine of Norman Bethune Medical Department Changchun 
      China.
FAU - Liang, W Z
AU  - Liang WZ
AD  - Jilin University Department of Neurology, China-Japan Union Hospital Changchun 
      China.
FAU - He, J T
AU  - He JT
AD  - Jilin University Department of Neurology, China-Japan Union Hospital Changchun 
      China.
FAU - Cui, Y
AU  - Cui Y
AD  - Jilin University Department of Neurology, China-Japan Union Hospital Changchun 
      China.
FAU - Liu, H Y
AU  - Liu HY
AD  - Jilin University Department of Neurology, China-Japan Union Hospital Changchun 
      China.
FAU - Xue, L X
AU  - Xue LX
AD  - Jilin University Department of Neurology, China-Japan Union Hospital Changchun 
      China.
FAU - Shi, W
AU  - Shi W
AD  - Jilin University Key Laboratory for Molecular Enzymology & Engineering, The 
      Ministry of Education Changchun China.
FAU - Shao, Y K
AU  - Shao YK
AD  - Jilin University Department of Neurology, China-Japan Union Hospital Changchun 
      China.
FAU - Mang, J
AU  - Mang J
AD  - Jilin University Department of Neurology, China-Japan Union Hospital Changchun 
      China mangjing@jlu.edu.cn.
FAU - Xu, Z X
AU  - Xu ZX
AD  - Jilin University Department of Neurology, China-Japan Union Hospital Changchun 
      China xuzhongxin999@aliyun.com.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20160229
PL  - France
TA  - Cell Mol Biol (Noisy-le-grand)
JT  - Cellular and molecular biology (Noisy-le-Grand, France)
JID - 9216789
RN  - 0 (Anthracenes)
RN  - 0 (Smad Proteins)
RN  - 0 (Transforming Growth Factor beta)
RN  - 0 (activin A)
RN  - 104625-48-1 (Activins)
RN  - 1TW30Y2766 (pyrazolanthrone)
RN  - 9061-61-4 (Nerve Growth Factor)
RN  - EC 2.7.11.24 (JNK Mitogen-Activated Protein Kinases)
RN  - IY9XDZ35W2 (Glucose)
RN  - S88TT14065 (Oxygen)
SB  - IM
MH  - Activins/*pharmacology
MH  - Animals
MH  - Anthracenes/pharmacology
MH  - Blotting, Western
MH  - Cell Differentiation/drug effects
MH  - *Cell Hypoxia
MH  - Cell Survival/drug effects
MH  - Epithelial-Mesenchymal Transition/drug effects
MH  - Glucose/*pharmacology
MH  - JNK Mitogen-Activated Protein Kinases/antagonists & inhibitors/*metabolism
MH  - Microscopy, Fluorescence
MH  - Nerve Growth Factor/pharmacology
MH  - Oxygen/*metabolism
MH  - PC12 Cells
MH  - Phosphorylation/drug effects
MH  - Rats
MH  - Signal Transduction/*drug effects
MH  - Smad Proteins/metabolism
MH  - Transforming Growth Factor beta/pharmacology
EDAT- 2016/03/08 06:00
MHDA- 2016/12/15 06:00
CRDT- 2016/03/08 06:00
PHST- 2015/11/13 00:00 [received]
PHST- 2016/02/26 00:00 [accepted]
PHST- 2016/03/08 06:00 [entrez]
PHST- 2016/03/08 06:00 [pubmed]
PHST- 2016/12/15 06:00 [medline]
PST - epublish
SO  - Cell Mol Biol (Noisy-le-grand). 2016 Feb 29;62(2):81-6.