PMID- 25516511
OWN - NLM
STAT- MEDLINE
DCOM- 20150726
LR  - 20191210
IS  - 0371-0874 (Print)
IS  - 0371-0874 (Linking)
VI  - 66
IP  - 6
DP  - 2014 Dec 25
TI  - The role of Toll-like receptor 4 on inflammation and Abeta formation in cortex 
      astrocytes.
PG  - 631-8
AB  - To investigate the role and possible molecular mechanism of astrocytes in 
      inflammation and amyloid beta-protein (Abeta) formation, in this research, by using LPS 
      to stimulate cultured rat astrocytes in vitro with or without anti-Toll-like 
      receptor 4 (TLR4) antibody pretreatment, we first detected the TLR4, TNF-alpha, 
      IL-1beta, beta-amyloid precursor protein (beta-APP) and beta-site APP clearing enzyme 1 
      (BACE1) mRNA with real-time PCR, and TLR4, NF-kappaB/P65 protein in cultured 
      astrocytes by Western blot, and then further probed the translocation of 
      NF-kappaB/P65 using immunofluorescence and the contents of TNF-alpha, IL-1beta and Abeta in 
      culture supernatant through ELISA. We found that all of these indexes increased 
      at different degrees after LPS-stimulation. However, if pretreatment with anti- 
      TLR4 antibody, such stimulating effects of LPS on the nuclear translocation of 
      NF-kappaB/P65 and TNF-alpha, IL-1beta, Abeta contents in astrocytic culture supernatant were 
      reduced significantly or disappeared in comparison with the group with only 
      LPS-administration. Our results suggest that TLR4 in astrocytes might play an 
      important role in the inflammation and Abeta formation through the TLR4/NF-kappaB 
      signaling pathway, thus providing new knowledge and understanding of the 
      inflammatory hypothesis of AD pathogenesis.
FAU - Gong, Chang-Yin
AU  - Gong CY
AD  - Department of Pathophysiology, Medical School of Nantong University, Nantong 
      226001, China; Department of Pathology, Affiliated Changzhou No. 2 People's 
      Hospital, Nanjing Medical University, Changzhou 213003, China; Evidence-based 
      Medicine Center, Medical School of Nantong University, Nantong 226001, China. 
      alz@ntu.edu.cn.
FAU - Zhou, Ai-Ling
AU  - Zhou AL
FAU - Mao, Jia-Hui
AU  - Mao JH
FAU - Hu, Ya-E
AU  - Hu YE
FAU - Geng, Jin-Song
AU  - Geng JS
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - China
TA  - Sheng Li Xue Bao
JT  - Sheng li xue bao : [Acta physiologica Sinica]
JID - 20730130R
RN  - 0 (Amyloid beta-Protein Precursor)
RN  - 0 (Interleukin-1beta)
RN  - 0 (RNA, Messenger)
RN  - 0 (Rela protein, rat)
RN  - 0 (Tlr4 protein, rat)
RN  - 0 (Toll-Like Receptor 4)
RN  - 0 (Transcription Factor RelA)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - EC 3.4.- (Amyloid Precursor Protein Secretases)
RN  - EC 3.4.23.- (Aspartic Acid Endopeptidases)
RN  - EC 3.4.23.46 (Bace1 protein, rat)
SB  - IM
MH  - Amyloid Precursor Protein Secretases/metabolism
MH  - Amyloid beta-Protein Precursor/metabolism
MH  - Animals
MH  - Aspartic Acid Endopeptidases/metabolism
MH  - Astrocytes/*metabolism
MH  - Cells, Cultured
MH  - Cerebral Cortex/cytology
MH  - Inflammation/*metabolism
MH  - Interleukin-1beta/metabolism
MH  - RNA, Messenger
MH  - Rats
MH  - Real-Time Polymerase Chain Reaction
MH  - *Signal Transduction
MH  - Toll-Like Receptor 4/*metabolism
MH  - Transcription Factor RelA/metabolism
MH  - Tumor Necrosis Factor-alpha/metabolism
EDAT- 2014/12/18 06:00
MHDA- 2015/07/28 06:00
CRDT- 2014/12/18 06:00
PHST- 2014/12/18 06:00 [entrez]
PHST- 2014/12/18 06:00 [pubmed]
PHST- 2015/07/28 06:00 [medline]
PST - ppublish
SO  - Sheng Li Xue Bao. 2014 Dec 25;66(6):631-8.