PMID- 17574273
OWN - NLM
STAT- MEDLINE
DCOM- 20070830
LR  - 20181113
IS  - 0022-4804 (Print)
IS  - 1095-8673 (Electronic)
IS  - 0022-4804 (Linking)
VI  - 141
IP  - 2
DP  - 2007 Aug
TI  - TNF-alpha and shear stress-induced large artery adaptations.
PG  - 299-305
AB  - BACKGROUND: Tumor necrosis factor-alpha (TNF-alpha) up-regulation has been 
      associated with both low and high shear-induced arterial remodeling. To address 
      this apparent paradox and to define the biology of TNF-alpha signaling in large 
      arteries, we tested the hypotheses that differential temporal expression of 
      TNF-alpha drives shear-regulated arterial remodeling. MATERIALS AND METHODS: Both 
      low- and high-shear environments in the same rabbit were surgically created for 
      common carotid arteries. Common carotid arteries (n = 60 total) were harvested 
      after d0, d1, d3, d7, and d14 and analyses included morphology, TNF-alpha, and 
      IL-10 mRNA quantitation. In separate experiments, animals received pegylated 
      soluble TNF-alpha Type 1 receptor (PEG sTNF-RI) or vehicle via either short- or 
      long-term dosing to define the effect of TNF-alpha blockade. RESULTS: The model 
      yielded a 14-fold shear differential (P < 0.001) with medial thickening under low 
      shear (P = 0.025), and evidence of outward remodeling with high shear (P = 
      0.007). Low shear immediately up-regulated TNF-alpha expression approximately 50 
      fold (P < 0.001) at d1. Conversely, high shear-induced delayed and sustained 
      TNF-alpha expression (22-fold at d7, P = 0.012; 23-fold at d14, P = 0.007). Both 
      low and high shear gradually induced IL-10 expression (P = 0.002 and P = 0.004, 
      respectively). Neither short-term (5-day) nor long-term (14-day) blockage of 
      TNF-alpha signaling resulted in treatment-induced changes in the remodeling of 
      low- or high-shear arteries. CONCLUSIONS: Shear stress differentially and 
      temporally regulates TNF-alpha expression in remodeling large arteries. However, 
      TNF-alpha blockage did not substantially impact the final shear-induced 
      morphology, suggesting that large arteries can remodel in response to flow 
      perturbations independent of TNF-alpha signaling.
FAU - Ozaki, C Keith
AU  - Ozaki CK
AD  - University of Florida College of Medicine and the Malcom Randall VAMC, 
      Gainesville, Florida, USA. Ozaki@surgery.ufl.edu
FAU - Jiang, Zhihua
AU  - Jiang Z
FAU - Berceli, Scott A
AU  - Berceli SA
LA  - eng
GR  - 1R01HL079135-01/HL/NHLBI NIH HHS/United States
GR  - R01 HL079135/HL/NHLBI NIH HHS/United States
GR  - R01 HL079135-03/HL/NHLBI NIH HHS/United States
GR  - R01 HL079135-01/HL/NHLBI NIH HHS/United States
GR  - K08 HL004070/HL/NHLBI NIH HHS/United States
GR  - K08HL04070-01/HL/NHLBI NIH HHS/United States
GR  - R01 HL079135-02/HL/NHLBI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
DEP - 20070615
PL  - United States
TA  - J Surg Res
JT  - The Journal of surgical research
JID - 0376340
RN  - 0 (RNA, Messenger)
RN  - 0 (Receptors, Tumor Necrosis Factor, Type I)
RN  - 0 (Tumor Necrosis Factor Decoy Receptors)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 130068-27-8 (Interleukin-10)
RN  - 1IEO802L3J (recombinant human tumor necrosis factor-binding protein-1)
SB  - IM
MH  - *Adaptation, Physiological
MH  - Animals
MH  - Carotid Artery, Common/*physiology
MH  - Immunohistochemistry
MH  - Interleukin-10/genetics
MH  - Male
MH  - RNA, Messenger/analysis
MH  - Rabbits
MH  - Receptors, Tumor Necrosis Factor, Type I/analysis
MH  - Shear Strength
MH  - Tumor Necrosis Factor Decoy Receptors/analysis
MH  - Tumor Necrosis Factor-alpha/antagonists & inhibitors/genetics/*physiology
PMC - PMC2032015
MID - NIHMS27615
EDAT- 2007/06/19 09:00
MHDA- 2007/08/31 09:00
PMCR- 2008/08/01
CRDT- 2007/06/19 09:00
PHST- 2006/11/01 00:00 [received]
PHST- 2006/12/18 00:00 [revised]
PHST- 2006/12/29 00:00 [accepted]
PHST- 2007/06/19 09:00 [pubmed]
PHST- 2007/08/31 09:00 [medline]
PHST- 2007/06/19 09:00 [entrez]
PHST- 2008/08/01 00:00 [pmc-release]
AID - S0022-4804(07)00005-4 [pii]
AID - 10.1016/j.jss.2006.12.563 [doi]
PST - ppublish
SO  - J Surg Res. 2007 Aug;141(2):299-305. doi: 10.1016/j.jss.2006.12.563. Epub 2007 
      Jun 15.