PMID- 9104823
OWN - NLM
STAT- MEDLINE
DCOM- 19970514
LR  - 20231105
IS  - 0022-1007 (Print)
IS  - 1540-9538 (Electronic)
IS  - 0022-1007 (Linking)
VI  - 185
IP  - 7
DP  - 1997 Apr 7
TI  - RANTES and monocyte chemoattractant protein-1 (MCP-1) play an important role in 
      the inflammatory phase of crescentic nephritis, but only MCP-1 is involved in 
      crescent formation and interstitial fibrosis.
PG  - 1371-80
AB  - The involvement of chemokines in inflammation is well established, but their 
      functional role in disease progression, and particularly in the development of 
      fibrosis, is not yet understood. To investigate the functional role that the 
      chemokines monocyte chemoattractant protein-1 (MCP-1) and RANTES play in 
      inflammation and the progression to fibrosis during crescentic nephritis we have 
      developed and characterized a murine model for this syndrome. Significant 
      increases in T-lymphocytes and macrophages were observed within glomeruli and 
      interstitium, paralleled by an induction of mRNA expression of MCP-1 and RANTES, 
      early after disease initiation. Blocking the function of MCP-1 or RANTES resulted 
      in significant decreases in proteinuria as well as in numbers of infiltrating 
      leukocytes, indicating that both MCP-1 and RANTES (regulated upon activation in 
      normal T cells expressed and secreted) play an important role in the inflammatory 
      phase of crescentic nephritis. In addition, neutralization of MCP-1 resulted in a 
      dramatic decrease in both glomerular crescent formation and deposition of type I 
      collagen. These results highlight a novel role for MCP-1 in crescent formation 
      and development of interstitial fibrosis, and indicate that in addition to 
      recruiting inflammatory cells this chemokine is critically involved in 
      irreversible tissue damage.
FAU - Lloyd, C M
AU  - Lloyd CM
AD  - Department of Medicine, Boston University Medical Center, Massachusetts 02118, 
      USA.
FAU - Minto, A W
AU  - Minto AW
FAU - Dorf, M E
AU  - Dorf ME
FAU - Proudfoot, A
AU  - Proudfoot A
FAU - Wells, T N
AU  - Wells TN
FAU - Salant, D J
AU  - Salant DJ
FAU - Gutierrez-Ramos, J C
AU  - Gutierrez-Ramos JC
LA  - eng
GR  - R01 DK030932/DK/NIDDK NIH HHS/United States
GR  - HL 148675-02/HL/NHLBI NIH HHS/United States
GR  - CICYT PB93-0317/CI/NCPDCID CDC HHS/United States
GR  - DK30932/DK/NIDDK NIH HHS/United States
GR  - 087618/WT_/Wellcome Trust/United Kingdom
GR  - R56 DK030932/DK/NIDDK NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - J Exp Med
JT  - The Journal of experimental medicine
JID - 2985109R
RN  - 0 (Chemokine CCL2)
RN  - 0 (Chemokine CCL5)
RN  - 0 (RNA, Messenger)
RN  - 9007-34-5 (Collagen)
SB  - IM
MH  - Animals
MH  - *Chemokine CCL2
MH  - *Chemokine CCL5
MH  - Collagen/biosynthesis/genetics
MH  - Disease Models, Animal
MH  - Disease Progression
MH  - Fibrosis/etiology
MH  - Glomerulonephritis/*etiology
MH  - Immunohistochemistry
MH  - Kidney/pathology
MH  - Mice
MH  - Proteinuria
MH  - RNA, Messenger/analysis
PMC - PMC2196251
EDAT- 1997/04/07 00:00
MHDA- 1997/04/07 00:01
PMCR- 1997/10/07
CRDT- 1997/04/07 00:00
PHST- 1997/04/07 00:00 [pubmed]
PHST- 1997/04/07 00:01 [medline]
PHST- 1997/04/07 00:00 [entrez]
PHST- 1997/10/07 00:00 [pmc-release]
AID - 10.1084/jem.185.7.1371 [doi]
PST - ppublish
SO  - J Exp Med. 1997 Apr 7;185(7):1371-80. doi: 10.1084/jem.185.7.1371.