PMID- 22333467
OWN - NLM
STAT- MEDLINE
DCOM- 20121018
LR  - 20120215
IS  - 1001-0939 (Print)
IS  - 1001-0939 (Linking)
VI  - 34
IP  - 11
DP  - 2011 Nov
TI  - [Investigation of inflammatory responses of pulmonary microvascular endothelial 
      cells induced by lipopolysaccharide and mechanism].
PG  - 816-20
AB  - OBJECTIVE: Lipopolysaccharide (LPS) can activate pulmonary vascular endothelial 
      cells (PMVECs) and induce inflammatory injury. Toll-like receptor-4 (TLR-4) is 
      integrally involved in LPS signaling and has a requisite role in the activation 
      of NF-kappaB. NF-kappaB is a key intercellular signaling event that mediates cell 
      inflammatory responses. The aim of the study was to investigate in an in vitro 
      model the inflammatory responses of PMVECs induced by LPS and the probable 
      mechanism underlying the observed inflammatory responses. METHODS: The present 
      study was performed on isolated PMVECs from Sprague-Dawley rats. After being 
      identified, PMVECs were divided into 2 groups: a control group, and a LPS (0.01, 
      0.1, 1, 10 mg/L) intervention group. ICAM-1, TNF-alpha and IL-8 were detected by 
      ELISA or radioimmunological methods. The expression of TLR-4 mRNA was detected by 
      real time PCR. The activation of NF-kappaB was detected by Western blot (proteins of 
      I-kappaBalpha and NF-kappaB p65) and immunocytochemical staining (NF-kappaB p65). RESULTS: 
      Compared with the control group, cytokines secreted from PMVECs-stimulated by LPS 
      were increased in a dose-dependent manner. When stimulated with LPS 10 mg/L for 
      2, 6 and 12 h, cytokines measured were all increased. ICAM-1 and TNF-alpha were 
      significantly increased and peaked after 2 h before gradually declining at 6 and 
      12 h. IL-8 was higher after 2 h, which continued up to 12 h. The expression of 
      TLR-4 mRNA was significantly higher and peaked after 2 h and continued to 12 h 
      (4.34 +/- 1.42, 3.62 +/- 1.45, 3.32 +/- 1.36), which were all higher than that of the 
      control group (1.00 +/- 0.00, P < 0.05). Meanwhile, NF-kappaB was activated at 0.5, 2, 
      6 and 12 h indicated by the significant degradation of IkappaB-alpha and the significant 
      increased release of NF-kappaB P65 and its subsequent translocation into the nucleus 
      with approximately synchronized. CONCLUSION: Taken together, the results 
      demonstrated that LPS was able to induce PMVECs inflammatory injury via 
      activating TLR-4 and subsequently activating NF-kappaB.
FAU - Xu, Shu-feng
AU  - Xu SF
AD  - Department of Respiratory Medicine, PLA General Hospital, Beijing 100853, China.
FAU - Wang, Ping
AU  - Wang P
FAU - Liang, Zhi-xin
AU  - Liang ZX
FAU - Sun, Ji-ping
AU  - Sun JP
FAU - Zhao, Xiao-wei
AU  - Zhao XW
FAU - Li, Ai-min
AU  - Li AM
FAU - Chen, Liang-an
AU  - Chen LA
LA  - chi
PT  - English Abstract
PT  - Journal Article
PL  - China
TA  - Zhonghua Jie He He Hu Xi Za Zhi
JT  - Zhonghua jie he he hu xi za zhi = Zhonghua jiehe he huxi zazhi = Chinese journal 
      of tuberculosis and respiratory diseases
JID - 8712226
RN  - 0 (Lipopolysaccharides)
RN  - 0 (NF-kappa B)
RN  - 0 (Tlr4 protein, rat)
RN  - 0 (Toll-Like Receptor 4)
SB  - IM
MH  - Animals
MH  - Cells, Cultured
MH  - Endothelial Cells/*drug effects/*metabolism
MH  - Inflammation/*metabolism
MH  - Lipopolysaccharides/*adverse effects
MH  - Lung/blood supply
MH  - NF-kappa B/metabolism
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Toll-Like Receptor 4/metabolism
EDAT- 2012/02/16 06:00
MHDA- 2012/10/19 06:00
CRDT- 2012/02/16 06:00
PHST- 2012/02/16 06:00 [entrez]
PHST- 2012/02/16 06:00 [pubmed]
PHST- 2012/10/19 06:00 [medline]
PST - ppublish
SO  - Zhonghua Jie He He Hu Xi Za Zhi. 2011 Nov;34(11):816-20.