PMID- 12080327
OWN - NLM
STAT- MEDLINE
DCOM- 20020806
LR  - 20191106
IS  - 0022-2143 (Print)
IS  - 0022-2143 (Linking)
VI  - 140
IP  - 1
DP  - 2002 Jul
TI  - Expression of monocyte chemoattractant protein-1 in proximal tubular epithelial 
      cells in a rat model of progressive kidney failure.
PG  - 43-51
AB  - Impairment of kidney function in various types of glomerular disease is 
      associated with tubulointerstitial changes. Monocyte chemoattractant protein-1 
      (MCP-1) is up-regulated in the tubulointerstitium and in the glomeruli in many 
      human and experimental kidney disorders. We investigated the localization of 
      MCP-1 expression in a rat model of progressive kidney failure. Male Wistar rats 
      were subjected to subtotal nephrectomy (n = 30) or sham surgery (n = 30). 
      Immunohistochemistry with immunoelectron microscopy and in situ hybridization 
      were used to examine the expression of MCP-1 protein and messenger ribonucleic 
      acid (mRNA) in the kidney, respectively. MCP-1 protein and mRNA were hardly 
      detected in both glomeruli and tubulointerstitium of control rats. However, in 
      the rats subjected to nephrectomy, MCP-1 expression was increased in the tubular 
      cells of the remnant kidney, accompanied by significant macrophage infiltration. 
      MCP-1 was observed mainly in the proximal tubular cells and only weakly in distal 
      tubular cells. No significant expression of MCP-1 protein or mRNA was noted in 
      the glomeruli. Immunoelectron microscopy showed the presence of MCP-1 in the 
      rough endoplasmic reticulum of proximal tubular cells, confirming that MCP-1 is 
      produced in proximal tubular cells. MCP-1 was also observed in endocytic vesicles 
      adjacent to the brush border of proximal tubular cells, suggesting incorporation 
      of MCP-1 from the tubular lumen. Our findings indicate localized expression of 
      MCP-1 in proximal tubular cells in the remnant kidney and suggest that MCP-1 in 
      proximal tubular cells is involved in tubulointerstitial damage in chronic kidney 
      failure associated with glomerular hypertension.
FAU - Ota, Takayuki
AU  - Ota T
AD  - Second Department of Internal Medicine, School of Medicine, University of 
      Occupational and Environmental Health, Yahatanishi, Kitakyushu, Japan.
FAU - Tamura, Masahito
AU  - Tamura M
FAU - Osajima, Akihiko
AU  - Osajima A
FAU - Doi, Yoshiaki
AU  - Doi Y
FAU - Kudo, Hideaki
AU  - Kudo H
FAU - Anai, Hirofumi
AU  - Anai H
FAU - Miyazaki, Masanobu
AU  - Miyazaki M
FAU - Nishino, Tomoya
AU  - Nishino T
FAU - Nakashima, Yasuhide
AU  - Nakashima Y
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - J Lab Clin Med
JT  - The Journal of laboratory and clinical medicine
JID - 0375375
RN  - 0 (Chemokine CCL2)
SB  - IM
MH  - Animals
MH  - Chemokine CCL2/*genetics
MH  - Disease Models, Animal
MH  - Disease Progression
MH  - Kidney Tubules/pathology/*physiopathology/ultrastructure
MH  - Male
MH  - Microscopy, Immunoelectron
MH  - Nephrectomy
MH  - Rats
MH  - Rats, Wistar
MH  - Renal Insufficiency/*genetics/pathology
MH  - Urothelium/pathology/*physiopathology/ultrastructure
EDAT- 2002/06/25 10:00
MHDA- 2002/08/07 10:01
CRDT- 2002/06/25 10:00
PHST- 2002/06/25 10:00 [pubmed]
PHST- 2002/08/07 10:01 [medline]
PHST- 2002/06/25 10:00 [entrez]
AID - S0022214302000161 [pii]
AID - 10.1067/mlc.2002.125215 [doi]
PST - ppublish
SO  - J Lab Clin Med. 2002 Jul;140(1):43-51. doi: 10.1067/mlc.2002.125215.