PMID- 9176841
OWN - NLM
STAT- MEDLINE
DCOM- 19970812
LR  - 20210518
IS  - 1046-6673 (Print)
IS  - 1046-6673 (Linking)
VI  - 8
IP  - 5
DP  - 1997 May
TI  - Renal expression of monocyte chemoattractant protein-1 in lupus autoimmune mice.
PG  - 720-9
AB  - Mononuclear cell infiltration in glomeruli and renal interstitium is a prominent 
      feature of some types of glomerulonephritis, including lupus nephritis. The 
      mechanism(s) underlying monocyte influx into the kidney is not fully understood. 
      Recently, monocyte chemoattractant protein-1 (MCP-1) has been identified as a 
      chemotactic factor involved in the recruitment of monocytes/macrophages in the 
      glomeruli of rats with mesangioproliferative as well as anti-glomerular basement 
      membrane glomerulonephritis. In the study presented here, renal MCP-1 mRNA 
      expression in New Zealand Black x New Zealand White (NZB/W) F1 mice, a model of 
      genetically determined immune complex disease that mimics systemic lupus in 
      humans, was investigated. Northern blot analysis revealed a single 0.7 kb MCP-1 
      transcript of very low intensity in kidneys from 2-month-old NZB/W mice that had 
      not yet developed proteinuria nor renal damage. Message levels, which increased 
      markedly with the progression of nephritis and in association with mononuclear 
      cell infiltration, were 10- and 15- fold higher in 8-10-month-old mice than in 
      2-month-old mice. By in situ hybridization, increased expression of MCP-1 mRNA 
      was demonstrated in glomeruli and, even more striking, in tubular epithelial 
      cells. Western blot analysis demonstrated increased expression of MCP-1 protein 
      in kidneys of 10-month-old NZB/W mice, consistent with MCP-1 mRNA data. When 
      NZB/W mice were treated with cyclophosphamide up to 12 months of age, expression 
      of MCP-1 in the renal tissue remained low, the influx of inflammatory cells did 
      not appear, and glomerular and tubular structures remained well preserved. These 
      data suggest that elevated MCP-1 might act as a signal for inflammatory cells to 
      infiltrate the kidney in lupus nephritis.
FAU - Zoja, C
AU  - Zoja C
AD  - Mario Negri Institute for Pharmacological Research, Bergamo, Italy.
FAU - Liu, X H
AU  - Liu XH
FAU - Donadelli, R
AU  - Donadelli R
FAU - Abbate, M
AU  - Abbate M
FAU - Testa, D
AU  - Testa D
FAU - Corna, D
AU  - Corna D
FAU - Taraboletti, G
AU  - Taraboletti G
FAU - Vecchi, A
AU  - Vecchi A
FAU - Dong, Q G
AU  - Dong QG
FAU - Rollins, B J
AU  - Rollins BJ
FAU - Bertani, T
AU  - Bertani T
FAU - Remuzzi, G
AU  - Remuzzi G
LA  - eng
PT  - Journal Article
PL  - United States
TA  - J Am Soc Nephrol
JT  - Journal of the American Society of Nephrology : JASN
JID - 9013836
RN  - 0 (Chemokine CCL2)
RN  - 0 (Immunosuppressive Agents)
RN  - 8N3DW7272P (Cyclophosphamide)
SB  - IM
MH  - Animals
MH  - Autoimmune Diseases/*metabolism/pathology/physiopathology
MH  - Chemokine CCL2/genetics/*metabolism
MH  - Cyclophosphamide/pharmacology
MH  - Female
MH  - Gene Expression
MH  - Immunosuppressive Agents/pharmacology
MH  - In Situ Hybridization
MH  - Kidney/*metabolism/pathology/physiopathology
MH  - Lupus Vulgaris/*metabolism/pathology/physiopathology
MH  - Mice
MH  - Mice, Inbred NZB
MH  - Proteinuria/urine
MH  - Time Factors
EDAT- 1997/05/01 00:00
MHDA- 1997/05/01 00:01
CRDT- 1997/05/01 00:00
PHST- 1997/05/01 00:00 [pubmed]
PHST- 1997/05/01 00:01 [medline]
PHST- 1997/05/01 00:00 [entrez]
AID - 10.1681/ASN.V85720 [doi]
PST - ppublish
SO  - J Am Soc Nephrol. 1997 May;8(5):720-9. doi: 10.1681/ASN.V85720.