PMID- 23554645
OWN - NLM
STAT- PubMed-not-MEDLINE
DCOM- 20130405
LR  - 20211021
IS  - 1674-8301 (Print)
IS  - 1674-8301 (Linking)
VI  - 24
IP  - 4
DP  - 2010 Jul
TI  - Interleukin-13 inhibits cytokines synthesis by blocking nuclear factor-kappaB and 
      c-Jun N-terminal kinase in human mesangial cells.
PG  - 308-16
LID - 10.1016/S1674-8301(10)60043-7 [doi]
AB  - OBJECTIVE: Monocytes/macrophages, proinflammatory cytokines and chemokines are 
      important in the pathogenesis of glomerulonephritis. Interleukin (IL) -13 has 
      been shown to exert potent anti-inflammatory properties. This study was designed 
      to investigate the effect of IL-13 on the expression of proinflammatory 
      cytokines, chemokines and profibrogenic cytokines and the involved molecular 
      mechanism in cultured human mesangial cells (HMCs). METHODS: The expressions of 
      proinflammatory cytokines, chemokines and profibrogenic cytokines were determined 
      by ribonuclease protection assay (RPA). Activity of nuclear factor-kappa B 
      (NF-kappaB) and activator protein-1 (AP-1) was examined by electrophoretic mobility 
      shift assay (EMSA). NF-kappaB subunit p65 nuclear transportation and c-Jun N-terminal 
      kinase (JNK) activity were assayed by immunoblot. RESULTS: Recombinant IL-13 
      inhibited tumor necrosis factor-alpha (TNF-alpha), IL-1alpha, IL-1beta, monocyte chemoattractant 
      protein-1 (MCP-1), IL-8, and transforming growth factor-beta1 (TGF-beta1) mRNA 
      expressions in a dose-dependent manner. Lipopolysacchorides (LPS) dramatically 
      increased NF-kappaB DNA binding activity of HMCs, which was inhibited by IL-13 in a 
      dose-dependent manner. LPS-activated NF-kappaB contained p50 and p65 dimers, but not 
      c-Rel subunit. IL-13 blocked LPS-induced NF-kappaB subunit p65. LPS stimulated 
      JNK/AP-1 activation, which was inhibited by IL-13 in a dose-dependent manner. 
      CONCLUSION: IL-13 inhibits proinflammatory cytokines, chemokines, and 
      profibrogenic cytokines synthesis by blocking NF-kappaB and JNK/AP-1 activation. 
      These observations point to the importance of IL-13 in the modulation of 
      inflammatory processes in the renal glomerulus.
FAU - Zhu, Chunhua
AU  - Zhu C
AD  - Nanjing Children's Hospital Affiliated to Nanjing Medical University, Nanjing 
      210008, Jiangsu Province, China ; Institute of Pediatrics, Nanjing Medical 
      University, Nanjing 210029, Jiangsu Province, China.
FAU - Zhang, Aihua
AU  - Zhang A
FAU - Huang, Songming
AU  - Huang S
FAU - Ding, Guixia
AU  - Ding G
FAU - Pan, Xiaoqin
AU  - Pan X
FAU - Chen, Ronghua
AU  - Chen R
LA  - eng
PT  - Journal Article
PL  - China
TA  - J Biomed Res
JT  - Journal of biomedical research
JID - 101551157
PMC - PMC3596597
OTO - NOTNLM
OT  - inflammation
OT  - interleukin-13
OT  - mesangial cells
EDAT- 2010/07/01 00:00
MHDA- 2010/07/01 00:01
PMCR- 2010/07/01
CRDT- 2013/04/05 06:00
PHST- 2010/01/25 00:00 [received]
PHST- 2013/04/05 06:00 [entrez]
PHST- 2010/07/01 00:00 [pubmed]
PHST- 2010/07/01 00:01 [medline]
PHST- 2010/07/01 00:00 [pmc-release]
AID - jbr-24-04-308 [pii]
AID - 10.1016/S1674-8301(10)60043-7 [doi]
PST - ppublish
SO  - J Biomed Res. 2010 Jul;24(4):308-16. doi: 10.1016/S1674-8301(10)60043-7.