PMID- 19207862
OWN - NLM
STAT- MEDLINE
DCOM- 20090715
LR  - 20171116
IS  - 1440-1797 (Electronic)
IS  - 1320-5358 (Linking)
VI  - 14
IP  - 3
DP  - 2009 Apr
TI  - Role of NAD(P)H oxidase in transforming growth factor-beta1-induced monocyte 
      chemoattractant protein-1 and interleukin-6 expression in rat renal tubular 
      epithelial cells.
PG  - 302-10
LID - 10.1111/j.1440-1797.2008.01072.x [doi]
AB  - AIM: This study investigated the role of NAD(P)H oxidase in transforming growth 
      factor-beta1 (TGF-beta1)-induced reactive oxygen species (ROS) generation, 
      monocyte chemoattractant protein-1 (MCP-1), and interleukin-6 (IL-6) expression 
      in rat renal tubular epithelial NRK-52E cells. METHODS: The cells were treated 
      with 10 ng/mL TGF-beta1, either in the presence or absence of the NAD(P)H oxidase 
      inhibitor, diphenyleneiodonium (DPI), or short hairpin RNA (shRNA) suppressing 
      p67phox expression. Expression of NAD(P)H oxidase subunits, MCP-1, and IL-6 at 
      the mRNA levels was detected by reverse transcription polymerase chain reaction, 
      while expression of NAD(P)H oxidase subunit p67phox protein was analyzed by 
      western blot and MCP-1 by enzyme-linked immunosorbent assay. The cellular ROS 
      generation was visualized using 2',7'-dichlorodihydrofluorescein diacetate by 
      confocal microscopy. RESULTS: Compared to control, TGF-beta1 upregulated NAD(P)H 
      oxidase subunit p67phox mRNA by 3.59-fold (P < 0.01), but had no effect on 
      p22phox, gp91phox and p47phox NAD(P)H subunits. TGF-beta1 was also able to 
      significantly increase intracellular ROS (P < 0.05), MCP-1 (P < 0.01) and IL-6 (P 
      < 0.05) expression in NRK-52E cells. Further studies showed that generation of 
      ROS and upregulation of MCP-1 and IL-6 by TGF-beta1 were significantly blocked by 
      addition of DPI or shRNA-p67phox (P < 0.01), suggesting that these effects were 
      NAD(P)H oxidase-dependent. CONCLUSION: TGF-beta1 differentially regulates the 
      expression of NAD(P)H oxidase subunits and mediates MCP-1 and IL-6 expression in 
      rat renal tubular cells via the NAD(P)H oxidase/p67phox-dependent mechanism.
FAU - Zhang, Haiyan
AU  - Zhang H
AD  - Department of Nephrology, The First Affiliated Hospital, Sun Yat-sen University, 
      Guangzhou, Guangdong, China.
FAU - Jiang, Zongpei
AU  - Jiang Z
FAU - Chang, Jie
AU  - Chang J
FAU - Li, Xiaoyan
AU  - Li X
FAU - Zhu, Hengmei
AU  - Zhu H
FAU - Lan, Hui Y
AU  - Lan HY
FAU - Zhou, Shu-Feng
AU  - Zhou SF
FAU - Yu, Xueqing
AU  - Yu X
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20090203
PL  - Australia
TA  - Nephrology (Carlton)
JT  - Nephrology (Carlton, Vic.)
JID - 9615568
RN  - 0 (Chemokine CCL2)
RN  - 0 (Interleukin-6)
RN  - 0 (Phosphoproteins)
RN  - 0 (Reactive Oxygen Species)
RN  - 0 (Transforming Growth Factor beta1)
RN  - 0 (neutrophil cytosol factor 67K)
RN  - EC 1.6.3.- (NADPH Oxidases)
SB  - IM
MH  - Animals
MH  - Cells, Cultured
MH  - Chemokine CCL2/*genetics
MH  - Epithelial Cells/metabolism
MH  - Interleukin-6/*genetics
MH  - Kidney Tubules/*metabolism
MH  - NADPH Oxidases/*physiology
MH  - Phosphoproteins/physiology
MH  - Rats
MH  - Reactive Oxygen Species/metabolism
MH  - Signal Transduction
MH  - Transforming Growth Factor beta1/*pharmacology
EDAT- 2009/02/12 09:00
MHDA- 2009/07/16 09:00
CRDT- 2009/02/12 09:00
PHST- 2009/02/12 09:00 [entrez]
PHST- 2009/02/12 09:00 [pubmed]
PHST- 2009/07/16 09:00 [medline]
AID - NEP1072 [pii]
AID - 10.1111/j.1440-1797.2008.01072.x [doi]
PST - ppublish
SO  - Nephrology (Carlton). 2009 Apr;14(3):302-10. doi: 
      10.1111/j.1440-1797.2008.01072.x. Epub 2009 Feb 3.