PMID- 17210403
OWN - NLM
STAT- MEDLINE
DCOM- 20070208
LR  - 20161124
IS  - 0741-5214 (Print)
IS  - 0741-5214 (Linking)
VI  - 45
IP  - 1
DP  - 2007 Jan
TI  - Tumor necrosis factor-alpha and the early vein graft.
PG  - 169-76
AB  - BACKGROUND: Tumor necrosis factor-alpha (TNF-alpha) has been implicated in the 
      blood vessel wall response to hemodynamic forces. We hypothesized that TNF-alpha 
      activity drives neointimal hyperplasia (NIH) during vein graft arterialization 
      and that anti-TNF-alpha therapy would inhibit NIH. METHODS: Rabbits underwent 
      bilateral vein grafting using jugular vein. All distal branches except the 
      occipital artery were unilaterally ligated to create distinct flow environments 
      between the bilateral grafts. Vein grafts were harvested sequentially up to 28 
      days for TNF-alpha messenger RNA (mRNA) quantitation. In separate experiments, 
      animals received short-term or long-term dosing with pegylated soluble TNF-alpha 
      type I receptor (PEG sTNF-RI) or vehicle. After 14 to 28 days, grafts were 
      analyzed for morphometry, proliferation, apoptosis, and PEG sTNF-RI distribution. 
      RESULTS: Quantitative mRNA assay (TaqMan) revealed shear-dependent (P < .001) and 
      time-dependent (P < .001) TNF-alpha expression. TNF-alpha induction was maximal 
      at day 1 and gradually decreased over time, but was persistently elevated even 4 
      weeks later (P < .001). Low shear (associated with increased NIH) resulted in 
      significantly higher TNF-alpha mRNA expression (P = .03). PEG sTNF-RI was found 
      in high concentrations in the serum and localized to NIH. The high-flow and 
      low-flow vein grafts from treated animals demonstrated similar volumes of NIH 
      compared with controls. PEG-sTNF-RI had only modest impact on vascular wall cell 
      turnover, as reflected by terminal deoxynucleotide transferase-mediated deoxy 
      uridine triphosphate nick-end labeling (P = .064) and anti-Ki-67 (P = .12) 
      assays. CONCLUSIONS: Placement of a vein into the arterial circulation acutely 
      upregulates TNF-alpha; this expression level correlates with the degree of 
      subsequent NIH. Pharmacologic interruption of this signaling pathway has no 
      significant impact on NIH or wall cellular proliferation/apoptosis, suggesting 
      that early vein graft adaptations can proceed via TNF-alpha-independent 
      mechanisms.
FAU - Jiang, Zhihua
AU  - Jiang Z
AD  - University of Florida College of Medicine, Gainesville, FL. USA.
FAU - Shukla, Ankur
AU  - Shukla A
FAU - Miller, Brett L
AU  - Miller BL
FAU - Espino, Derek R
AU  - Espino DR
FAU - Tao, Ming
AU  - Tao M
FAU - Berceli, Scott A
AU  - Berceli SA
FAU - Ozaki, C Keith
AU  - Ozaki CK
LA  - eng
GR  - 1R01HL079135-01/HL/NHLBI NIH HHS/United States
GR  - K08 HL76453-01/HL/NHLBI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - J Vasc Surg
JT  - Journal of vascular surgery
JID - 8407742
RN  - 0 (RNA, Messenger)
RN  - 0 (Receptors, Tumor Necrosis Factor, Type I)
RN  - 0 (Recombinant Proteins)
RN  - 0 (Tumor Necrosis Factor Decoy Receptors)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 1IEO802L3J (recombinant human tumor necrosis factor-binding protein-1)
SB  - IM
MH  - Animals
MH  - Apoptosis/*physiology
MH  - *Blood Vessel Prosthesis
MH  - Cell Proliferation
MH  - Disease Models, Animal
MH  - Graft Survival
MH  - Hyperplasia/metabolism/pathology
MH  - Jugular Veins/*metabolism/pathology/*transplantation
MH  - Male
MH  - RNA, Messenger/*genetics
MH  - Rabbits
MH  - Receptors, Tumor Necrosis Factor, Type I/pharmacology
MH  - Recombinant Proteins/pharmacology
MH  - Reverse Transcriptase Polymerase Chain Reaction
MH  - Time Factors
MH  - Tumor Necrosis Factor Decoy Receptors/pharmacology
MH  - Tumor Necrosis Factor-alpha/*genetics/metabolism
MH  - Tunica Intima/pathology
MH  - *Up-Regulation
EDAT- 2007/01/11 09:00
MHDA- 2007/02/09 09:00
CRDT- 2007/01/11 09:00
PHST- 2006/06/30 00:00 [received]
PHST- 2006/08/23 00:00 [accepted]
PHST- 2007/01/11 09:00 [pubmed]
PHST- 2007/02/09 09:00 [medline]
PHST- 2007/01/11 09:00 [entrez]
AID - S0741-5214(06)01514-X [pii]
AID - 10.1016/j.jvs.2006.08.049 [doi]
PST - ppublish
SO  - J Vasc Surg. 2007 Jan;45(1):169-76. doi: 10.1016/j.jvs.2006.08.049.