PMID- 12517735
OWN - NLM
STAT- MEDLINE
DCOM- 20030514
LR  - 20171116
IS  - 1931-857X (Print)
IS  - 1522-1466 (Linking)
VI  - 284
IP  - 5
DP  - 2003 May
TI  - Involvement of ERK pathway in albumin-induced MCP-1 expression in mouse proximal 
      tubular cells.
PG  - F1037-45
AB  - Persistent proteinuria has been indicated to be a major risk factor for the 
      development of tubulointerstitial damage through a process of proinflammatory 
      molecule expression. Monocyte chemoattractant protein-1 (MCP-1) was shown to 
      contribute to recruitment of immune cells into the renal interstitium in acute 
      and chronic renal diseases. However, the molecular mechanisms by which 
      proteinuria causes MCP-1 expression in proximal tubular cells have not been fully 
      clarified. In this study, we examined whether albumin overload-induced MCP-1 
      expression was regulated by mitogen-activated protein kinase (MAPK) in mouse 
      proximal tubular (mProx) cells. Exposure of mProx cells to delipidated bovine 
      serum albumin (BSA) induced mRNA and protein expression of MCP-1 in a time- and 
      dose-dependent manner. BSA activated extracellular signal-regulated kinase 
      (ERK1/2) and p38 MAPK. The MEK inhibitor U-0126 partially suppressed BSA-induced 
      MCP-1 expression and MCP-1 promoter/luciferase reporter activity. U-0126 also 
      inhibited an increase in nuclear factor-kappaB and activator protein-1 
      DNA-binding activity of MCP-1 promoter by protein overload in mProx cells. In 
      addition, we found that U-0126 inhibited BSA-induced nuclear factor-kappaB 
      reporter activity and inhibitory protein degradation in mProx cells. In 
      conclusion, these findings indicate that ERK signaling is involved in BSA-induced 
      MCP-1 expression in mProx cells.
FAU - Takaya, Kiho
AU  - Takaya K
AD  - Department of Medicine, Shiga University of Medical Science, Shiga 520-2192, 
      Japan.
FAU - Koya, Daisuke
AU  - Koya D
FAU - Isono, Motohide
AU  - Isono M
FAU - Sugimoto, Toshiro
AU  - Sugimoto T
FAU - Sugaya, Takeshi
AU  - Sugaya T
FAU - Kashiwagi, Atsunori
AU  - Kashiwagi A
FAU - Haneda, Masakazu
AU  - Haneda M
LA  - eng
PT  - Journal Article
DEP - 20030107
PL  - United States
TA  - Am J Physiol Renal Physiol
JT  - American journal of physiology. Renal physiology
JID - 100901990
RN  - 0 (Chemokine CCL2)
RN  - 0 (I-kappa B Proteins)
RN  - 0 (NF-kappa B)
RN  - 0 (Protein Isoforms)
RN  - 0 (RNA, Messenger)
RN  - 0 (Transcription Factor AP-1)
RN  - 27432CM55Q (Serum Albumin, Bovine)
RN  - 9007-49-2 (DNA)
RN  - EC 2.7.11.24 (Mitogen-Activated Protein Kinases)
SB  - IM
MH  - Animals
MH  - Cell Transformation, Viral
MH  - Cells, Cultured
MH  - Chemokine CCL2/genetics/*metabolism
MH  - DNA/metabolism
MH  - Enzyme Activation/physiology
MH  - I-kappa B Proteins/metabolism
MH  - Kidney Tubules, Proximal/cytology/*metabolism
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Mitogen-Activated Protein Kinases/drug effects/*physiology
MH  - NF-kappa B/physiology
MH  - Protein Isoforms/metabolism
MH  - RNA, Messenger/metabolism
MH  - Serum Albumin, Bovine/*pharmacology
MH  - Transcription Factor AP-1/metabolism
EDAT- 2003/01/09 04:00
MHDA- 2003/05/15 05:00
CRDT- 2003/01/09 04:00
PHST- 2003/01/09 04:00 [pubmed]
PHST- 2003/05/15 05:00 [medline]
PHST- 2003/01/09 04:00 [entrez]
AID - 00230.2002 [pii]
AID - 10.1152/ajprenal.00230.2002 [doi]
PST - ppublish
SO  - Am J Physiol Renal Physiol. 2003 May;284(5):F1037-45. doi: 
      10.1152/ajprenal.00230.2002. Epub 2003 Jan 7.