PMID- 11012884
OWN - NLM
STAT- MEDLINE
DCOM- 20001113
LR  - 20220330
IS  - 0085-2538 (Print)
IS  - 0085-2538 (Linking)
VI  - 58
IP  - 4
DP  - 2000 Oct
TI  - Up-regulation of monocyte chemoattractant protein-1 in tubulointerstitial lesions 
      of human diabetic nephropathy.
PG  - 1492-9
AB  - BACKGROUND: We previously described that monocyte chemoattractant protein-1 
      (MCP-1) plays an important role in progressive glomerular and interstitial damage 
      in inflammatory renal diseases. However, the expression of MCP-1 in diabetic 
      nephropathy remains to be investigated. METHODS: We examined whether locally 
      expressed MCP-1 participates in human diabetic nephropathy via recruiting and 
      activating monocytes/macrophages (Mphi). Urinary and serum MCP-1 levels were 
      measured by enzyme-linked immunosorbent assay in 45 patients with diabetic 
      nephropathy. The presence of MCP-1 in diseased kidneys was determined by 
      immunohistochemical and in situ hybridization analyses. RESULTS: Urinary MCP-1 
      levels were significantly elevated in patients with diabetic nephrotic syndrome 
      and advanced tubulointerstitial lesions. Moreover, urinary levels of MCP-1 were 
      well correlated with the number of CD68-positive infiltrating cells in the 
      interstitium. In contrast, serum MCP-1 levels remained similar to those of 
      healthy volunteers. Furthermore, we detected the MCP-1-positive cells in the 
      interstitium of diabetic nephropathy via both immunohistochemical and in situ 
      hybridization analyses. CONCLUSION: These observations suggest that locally 
      produced MCP-1 may be involved in the development of advanced diabetic 
      nephropathy, especially in the formation of tubulointerstitial lesions possibly 
      through Mphi recruitment and activation. Moreover, up-regulation of MCP-1 may be 
      a common pathway involved in the progressive tubulointerstitial damage in 
      diabetic nephropathy as well as inflammatory renal diseases.
FAU - Wada, T
AU  - Wada T
AD  - First Department of Internal Medicine and Division of Blood Purification, School 
      of Medicine, and Department of Molecular Oncology, Cancer Research Institute, 
      Kanazawa University, Kanazawa, Japan. twada@medf.m.knazawa-u.ac.jp
FAU - Furuichi, K
AU  - Furuichi K
FAU - Sakai, N
AU  - Sakai N
FAU - Iwata, Y
AU  - Iwata Y
FAU - Yoshimoto, K
AU  - Yoshimoto K
FAU - Shimizu, M
AU  - Shimizu M
FAU - Takeda, S I
AU  - Takeda SI
FAU - Takasawa, K
AU  - Takasawa K
FAU - Yoshimura, M
AU  - Yoshimura M
FAU - Kida, H
AU  - Kida H
FAU - Kobayashi, K I
AU  - Kobayashi KI
FAU - Mukaida, N
AU  - Mukaida N
FAU - Naito, T
AU  - Naito T
FAU - Matsushima, K
AU  - Matsushima K
FAU - Yokoyama, H
AU  - Yokoyama H
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Kidney Int
JT  - Kidney international
JID - 0323470
RN  - 0 (Chemokine CCL2)
RN  - 0 (RNA, Messenger)
RN  - 0 (Transforming Growth Factor beta)
SB  - IM
MH  - Adolescent
MH  - Adult
MH  - Aged
MH  - Aged, 80 and over
MH  - Cell Movement/immunology
MH  - Chemokine CCL2/*genetics/*urine
MH  - Diabetic Nephropathies/pathology/*physiopathology/urine
MH  - Female
MH  - Gene Expression/physiology
MH  - Humans
MH  - In Situ Hybridization
MH  - Macrophages/cytology/metabolism
MH  - Male
MH  - Middle Aged
MH  - Monocytes/cytology/metabolism
MH  - Nephritis, Interstitial/pathology/*physiopathology/urine
MH  - RNA, Messenger/analysis
MH  - Transcription, Genetic/physiology
MH  - Transforming Growth Factor beta/metabolism
MH  - Up-Regulation/genetics
EDAT- 2000/09/30 11:00
MHDA- 2001/02/28 10:01
CRDT- 2000/09/30 11:00
PHST- 2000/09/30 11:00 [pubmed]
PHST- 2001/02/28 10:01 [medline]
PHST- 2000/09/30 11:00 [entrez]
AID - S0085-2538(15)47248-5 [pii]
AID - 10.1046/j.1523-1755.2000.00311.x [doi]
PST - ppublish
SO  - Kidney Int. 2000 Oct;58(4):1492-9. doi: 10.1046/j.1523-1755.2000.00311.x.