PMID- 23479382
OWN - NLM
STAT- MEDLINE
DCOM- 20131104
LR  - 20211021
IS  - 1573-4919 (Electronic)
IS  - 0300-8177 (Linking)
VI  - 378
IP  - 1-2
DP  - 2013 Jun
TI  - Signaling pathways regulating dose-dependent dual effects of TNF-alpha on primary 
      cultured Schwann cells.
PG  - 237-46
LID - 10.1007/s11010-013-1614-x [doi]
AB  - After peripheral nerve injury, Schwann cells are rapidly activated to participate 
      in the regenerative process and modulate local immune reactions. Tumor necrosis 
      factor-alpha (TNF-alpha), one of the major initiators of the inflammatory cascade, has 
      been known to exert pleiotropic functions during peripheral nerve injury and 
      regeneration. In this study, we aimed to investigate the in vitro effects of 
      TNF-alpha on peripheral neural cells. First, gene-microarray analysis was applied to 
      the RNA samples extracted from injured peripheral nerves, providing the 
      information of gene interactions post nerve injury. Then, after primary cultured 
      Schwann cells were treated with increasing dosages (0-40 ng/ml) of TNF-alpha, cell 
      proliferation and migration were examined by EdU incorporation and a 
      transwell-based assay, and cell apoptosis was observed and quantified by electron 
      microscopy and Annexin V-FITC assay, respectively. The results showed that lower 
      dosages of TNF-alpha increased cell proliferation and migration, whereas higher 
      dosages of TNF-alpha decreased cell proliferation and migration and enhanced cell 
      apoptosis. The tests using a chemical inhibitor of TNF-alpha further confirmed the 
      above effects of TNF-alpha. To understand how TNF-alpha produced the dose-dependent dual 
      effects on primary cultured Schwann cells, we performed co-immunoprecipitation, 
      Western blot analysis, and immunocytochemistry to decipher the complex network of 
      biochemical pathways involving many signaling molecules, i.e., TNF 
      receptor-associated death domain, Fas-associated death domain, receptor 
      interacting protein, JNK, NF-kappaB p65, and caspases, thus assuming the mechanisms 
      by which TNF-alpha activated the death and survival pathways and achieved a balance 
      between the two opposite actions in primary cultured Schwann cells.
FAU - Tang, Xin
AU  - Tang X
AD  - School of Biology and Basic Medical Sciences, Soochow University, Suzhou, China.
FAU - Wang, Yongjun
AU  - Wang Y
FAU - Zhou, Songlin
AU  - Zhou S
FAU - Qian, Tianmei
AU  - Qian T
FAU - Gu, Xiaosong
AU  - Gu X
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20130312
PL  - Netherlands
TA  - Mol Cell Biochem
JT  - Molecular and cellular biochemistry
JID - 0364456
RN  - 0 (Fas-Associated Death Domain Protein)
RN  - 0 (NF-kappa B)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - EC 2.7.11.1 (Receptor-Interacting Protein Serine-Threonine Kinases)
RN  - EC 2.7.11.24 (JNK Mitogen-Activated Protein Kinases)
RN  - EC 3.4.22.- (Caspases)
SB  - IM
MH  - Animals
MH  - Apoptosis
MH  - Caspases/metabolism
MH  - Cell Movement
MH  - Cell Proliferation
MH  - Cell Shape
MH  - Cell Survival
MH  - Cells, Cultured
MH  - Fas-Associated Death Domain Protein/metabolism
MH  - JNK Mitogen-Activated Protein Kinases/metabolism
MH  - Male
MH  - NF-kappa B/metabolism
MH  - Phosphorylation
MH  - Primary Cell Culture
MH  - Protein Processing, Post-Translational
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Receptor-Interacting Protein Serine-Threonine Kinases/metabolism
MH  - Schwann Cells/*metabolism/physiology/ultrastructure
MH  - *Signal Transduction
MH  - Transcriptome
MH  - Tumor Necrosis Factor-alpha/*physiology
EDAT- 2013/03/13 06:00
MHDA- 2013/11/05 06:00
CRDT- 2013/03/13 06:00
PHST- 2012/11/07 00:00 [received]
PHST- 2013/03/02 00:00 [accepted]
PHST- 2013/03/13 06:00 [entrez]
PHST- 2013/03/13 06:00 [pubmed]
PHST- 2013/11/05 06:00 [medline]
AID - 10.1007/s11010-013-1614-x [doi]
PST - ppublish
SO  - Mol Cell Biochem. 2013 Jun;378(1-2):237-46. doi: 10.1007/s11010-013-1614-x. Epub 
      2013 Mar 12.