PMID- 11701464
OWN - NLM
STAT- MEDLINE
DCOM- 20011207
LR  - 20190901
IS  - 1524-4636 (Electronic)
IS  - 1079-5642 (Linking)
VI  - 21
IP  - 11
DP  - 2001 Nov
TI  - Pulsatile flow regulates monocyte adhesion to oxidized lipid-induced endothelial 
      cells.
PG  - 1770-6
AB  - Oxidized 1-palmitoyl-2-arachidonoyl-sn-glycero-3-phosphorylcholine (ox-PAPC), a 
      component of minimally modified low density lipoprotein, induces monocyte 
      adhesion to endothelial cells. It is not known whether the upstroke slopes of 
      pulsatile flow, defined as shear stress slew rates (tau(r)/tauT)), can regulate 
      monocyte binding to ox-PAPC-treated bovine aortic endothelial cells (BAECs). At 
      60 cycles per minute, ox-PAPC-treated BAECs were exposed to 3 conditions 
      representing known vascular conditions: (1) high shear stress slew rates 
      (tau(r)/tau(T)=293 dyne. cm(-2). s(-1)), with time-averaged shear stress=50 
      dyne/cm(2); (2) low shear stress slew rate (tau(r)/tau(t)=71 dyne. cm(-2). 
      s(-1)), with identical time-averaged shear stress; and (3) reversing oscillating 
      flow (0+/-2.6 mm Hg). Reverse transcription-polymerase chain reaction and 
      quantification were performed for monocyte chemoattractant protein-1 (MCP-1) mRNA 
      expression. High tau(r)/tau(t) reduced monocyte binding to ox-PAPC-treated BAECs 
      by 64+/-3.2% compared with static conditions, and low tau(r)/tau(t) reduced 
      monocyte binding by 31+/-3.4%, whereas oscillating flow increased monocyte 
      binding by 22+/-1.7% (P<0.005). High partial tau(r)/tau(t) downregulated MCP-1 
      expression by 33+/-8%, and low partial tau(r)/tau(t) downregulated MCP-1 
      expression by 15+/-4%, but oscillating flow upregulated MCP-1 by 13+/-5%. These 
      results suggest that shear stress slew rates regulate monocyte binding by 
      modulating the expression of a potent monocyte chemoattractant.
FAU - Hsiai, T K
AU  - Hsiai TK
AD  - Division of Cardiology, Department of Medicine, UCLA School of Medicine, UCLA 
      School of Engineering and Applied Sciences, Los Angeles, California, USA. 
      thsiai@mednet.ucla.edu
FAU - Cho, S K
AU  - Cho SK
FAU - Reddy, S
AU  - Reddy S
FAU - Hama, S
AU  - Hama S
FAU - Navab, M
AU  - Navab M
FAU - Demer, L L
AU  - Demer LL
FAU - Honda, H M
AU  - Honda HM
FAU - Ho, C M
AU  - Ho CM
LA  - eng
GR  - HL-07895/HL/NHLBI 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  - Arterioscler Thromb Vasc Biol
JT  - Arteriosclerosis, thrombosis, and vascular biology
JID - 9505803
RN  - 0 (Chemokine CCL2)
RN  - 0 (Lipoproteins, LDL)
RN  - 0 (Phosphatidylcholines)
RN  - 0 (RNA, Messenger)
RN  - 0 (oxidized low density lipoprotein)
SB  - IM
MH  - Animals
MH  - Cattle
MH  - *Cell Adhesion
MH  - Cells, Cultured
MH  - Chemokine CCL2/biosynthesis/genetics
MH  - Endothelium, Vascular/drug effects/metabolism/*physiology
MH  - Kinetics
MH  - Lipoproteins, LDL/*pharmacology
MH  - Monocytes/*physiology
MH  - Phosphatidylcholines/pharmacology
MH  - RNA, Messenger/biosynthesis
MH  - Stress, Mechanical
EDAT- 2001/11/10 10:00
MHDA- 2002/01/05 10:01
CRDT- 2001/11/10 10:00
PHST- 2001/11/10 10:00 [pubmed]
PHST- 2002/01/05 10:01 [medline]
PHST- 2001/11/10 10:00 [entrez]
AID - 10.1161/hq1001.097104 [doi]
PST - ppublish
SO  - Arterioscler Thromb Vasc Biol. 2001 Nov;21(11):1770-6. doi: 
      10.1161/hq1001.097104.