PMID- 21115617
OWN - NLM
STAT- MEDLINE
DCOM- 20110210
LR  - 20220318
IS  - 1533-3450 (Electronic)
IS  - 1046-6673 (Print)
IS  - 1046-6673 (Linking)
VI  - 22
IP  - 1
DP  - 2011 Jan
TI  - MCP-1 contributes to arteriovenous fistula failure.
PG  - 43-8
LID - 10.1681/ASN.2010040373 [doi]
AB  - Vascular access dysfunction compromises the care of patients on chronic 
      hemodialysis. Elucidating the mechanisms of such dysfunction and devising 
      strategies that may interrupt neointimal hyperplasia and relevant pathogenetic 
      pathways are essential. Here, we show that, in the venous segment of a murine 
      model of an arteriovenous fistula, monocyte chemoattractant protein-1 (MCP-1) 
      mRNA and protein increase, accompanied by increased activity of the transcription 
      factors NF-kappaB and AP-1. Genetic deficiency of MCP-1 proved markedly protective in 
      this murine model, reflected by increased fistula patency 6 weeks after its 
      formation, decreased venous wall thickness, and increased luminal area. An early 
      effect of MCP-1 deficiency was the attenuation of the marked induction of CCL5 
      (RANTES) that occurred in this model, a chemokine recently recognized as a 
      critical participant in vascular injury. Finally, in a rat model of an 
      arteriovenous fistula, we localized expression of MCP-1 to the endothelium, 
      proliferating smooth muscle cells and infiltrating leukocytes. In summary, marked 
      upregulation of MCP-1 occurs in the venous segment of an arteriovenous fistula in 
      rodents, and this vasculopathic chemokine contributes to failure of the fistula.
FAU - Juncos, Julio P
AU  - Juncos JP
AD  - Mayo Clinic, Guggenheim 542, 200 First Street, SW, Rochester, MN 55905, USA.
FAU - Grande, Joseph P
AU  - Grande JP
FAU - Kang, Lu
AU  - Kang L
FAU - Ackerman, Allan W
AU  - Ackerman AW
FAU - Croatt, Anthony J
AU  - Croatt AJ
FAU - Katusic, Zvonimir S
AU  - Katusic ZS
FAU - Nath, Karl A
AU  - Nath KA
LA  - eng
GR  - DK47060/DK/NIDDK NIH HHS/United States
GR  - R01 DK047060/DK/NIDDK NIH HHS/United States
GR  - R01 DK070124/DK/NIDDK NIH HHS/United States
GR  - DK70124/DK/NIDDK NIH HHS/United States
GR  - R37 DK047060/DK/NIDDK NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
DEP - 20101129
PL  - United States
TA  - J Am Soc Nephrol
JT  - Journal of the American Society of Nephrology : JASN
JID - 9013836
RN  - 0 (Ccl2 protein, mouse)
RN  - 0 (Ccl2 protein, rat)
RN  - 0 (Chemokine CCL2)
RN  - 0 (NF-kappa B)
RN  - 0 (Transcription Factor AP-1)
SB  - IM
MH  - Animals
MH  - Arteriovenous Shunt, Surgical/*adverse effects
MH  - Cell Proliferation
MH  - Chemokine CCL2/genetics/*metabolism
MH  - Endothelium, Vascular/cytology/*metabolism
MH  - Leukocytes/cytology
MH  - Male
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Mice, Knockout
MH  - Models, Animal
MH  - NF-kappa B/metabolism
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Renal Dialysis/methods
MH  - Transcription Factor AP-1/metabolism
MH  - Up-Regulation/*physiology
PMC - PMC3014033
EDAT- 2010/12/01 06:00
MHDA- 2011/02/11 06:00
PMCR- 2012/01/01
CRDT- 2010/12/01 06:00
PHST- 2010/12/01 06:00 [entrez]
PHST- 2010/12/01 06:00 [pubmed]
PHST- 2011/02/11 06:00 [medline]
PHST- 2012/01/01 00:00 [pmc-release]
AID - ASN.2010040373 [pii]
AID - 2010040373 [pii]
AID - 10.1681/ASN.2010040373 [doi]
PST - ppublish
SO  - J Am Soc Nephrol. 2011 Jan;22(1):43-8. doi: 10.1681/ASN.2010040373. Epub 2010 Nov 
      29.