PMID- 17068152
OWN - NLM
STAT- MEDLINE
DCOM- 20070320
LR  - 20210206
IS  - 0006-4971 (Print)
IS  - 1528-0020 (Electronic)
IS  - 0006-4971 (Linking)
VI  - 109
IP  - 5
DP  - 2007 Mar 1
TI  - Tumor necrosis factor alpha (TNF-alpha) receptor-II is required for 
      TNF-alpha-induced leukocyte-endothelial interaction in vivo.
PG  - 1938-44
AB  - Tumor necrosis factor-alpha (TNF-alpha) binds to 2 distinct cell-surface 
      receptors: TNF-alpha receptor-I (TNFR-I: p55) and TNF-alpha receptor-II (TNFR-II: 
      p75). TNF-alpha induces leukocyte adhesion molecules on endothelial cells (ECs), 
      which mediate 3 defined steps of the inflammatory response; namely, leukocyte 
      rolling, firm adhesion, and transmigration. In this study, we have investigated 
      the role of p75 in TNF-alpha-induced leukocyte adhesion molecules using cultured 
      ECs derived from wild-type (WT), p75-null (p75-/-), or p55-null (p55-/-) mice. We 
      observed that p75 was essential for TNF-alpha-induced E-selectin, vascular cell 
      adhesion molecule 1 (VCAM-1), and intercellular adhesion molecule 1 (ICAM-1) 
      expression. We also investigated the putative role of p75 in inflammation in vivo 
      using an intravital microscopic approach with a mouse cremaster muscle model. 
      TNF-alpha-stimulated leukocyte rolling, firm adhesion to ECs, and transmigration 
      were dramatically reduced in p75-/- mice. Transplanted WT cremaster in p75-/- 
      mice showed a robust leukocyte rolling and firm adhesion upon TNF-alpha 
      activation, suggesting that the impairment in EC-leukocyte interaction in p75-/- 
      mice is due to EC dysfunction. These results demonstrate, for the first time, 
      that endothelial p75 is essential for TNF-alpha-induced 
      leukocyte-endothelial-cell interaction. Our findings may contribute to the 
      identification of novel p75-targeted therapeutic approaches for inflammatory 
      diseases.
FAU - Chandrasekharan, Unni M
AU  - Chandrasekharan UM
AD  - Department of Cell Biology, Lerner Research Institute and Cleveland Clinic Lerner 
      College of Medicine of Case Western Reserve University, Cleveland Clinic 
      Foundation, OH 44195, USA.
FAU - Siemionow, Maria
AU  - Siemionow M
FAU - Unsal, Murat
AU  - Unsal M
FAU - Yang, Lin
AU  - Yang L
FAU - Poptic, Earl
AU  - Poptic E
FAU - Bohn, Justin
AU  - Bohn J
FAU - Ozer, Kagan
AU  - Ozer K
FAU - Zhou, Zhongmin
AU  - Zhou Z
FAU - Howe, Philip H
AU  - Howe PH
FAU - Penn, Marc
AU  - Penn M
FAU - DiCorleto, Paul E
AU  - DiCorleto PE
LA  - eng
GR  - M01 RR000080/RR/NCRR NIH HHS/United States
GR  - P01 HL029582/HL/NHLBI NIH HHS/United States
GR  - HL29582/HL/NHLBI NIH HHS/United States
GR  - RR-00080/RR/NCRR NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
DEP - 20061026
PL  - United States
TA  - Blood
JT  - Blood
JID - 7603509
RN  - 0 (E-Selectin)
RN  - 0 (Receptors, Tumor Necrosis Factor, Type II)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 0 (Vascular Cell Adhesion Molecule-1)
RN  - 126547-89-5 (Intercellular Adhesion Molecule-1)
SB  - IM
MH  - Animals
MH  - Blood Cell Count
MH  - Cell Adhesion
MH  - *Cell Communication
MH  - Cell Movement
MH  - E-Selectin/metabolism
MH  - Endothelial Cells/drug effects/*metabolism
MH  - Intercellular Adhesion Molecule-1/metabolism
MH  - Leukocytes/cytology/drug effects/*metabolism
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Mice, Knockout
MH  - Receptors, Tumor Necrosis Factor, Type II/deficiency/genetics/*metabolism
MH  - Tumor Necrosis Factor-alpha/*metabolism/pharmacology
MH  - Vascular Cell Adhesion Molecule-1/metabolism
PMC - PMC1801063
EDAT- 2006/10/28 09:00
MHDA- 2007/03/21 09:00
PMCR- 2008/03/01
CRDT- 2006/10/28 09:00
PHST- 2006/10/28 09:00 [pubmed]
PHST- 2007/03/21 09:00 [medline]
PHST- 2006/10/28 09:00 [entrez]
PHST- 2008/03/01 00:00 [pmc-release]
AID - S0006-4971(20)41915-9 [pii]
AID - 2006/020875 [pii]
AID - 10.1182/blood-2006-05-020875 [doi]
PST - ppublish
SO  - Blood. 2007 Mar 1;109(5):1938-44. doi: 10.1182/blood-2006-05-020875. Epub 2006 
      Oct 26.