Functional implications of tissue factor localization to cell-cell contacts in myocardium

Citation
T. Luther et al., Functional implications of tissue factor localization to cell-cell contacts in myocardium, J PATHOLOGY, 192(1), 2000, pp. 121-130
Citations number
55
Categorie Soggetti
Research/Laboratory Medicine & Medical Tecnology","Medical Research Diagnosis & Treatment
Journal title
JOURNAL OF PATHOLOGY
ISSN journal
00223417 → ACNP
Volume
192
Issue
1
Year of publication
2000
Pages
121 - 130
Database
ISI
SICI code
0022-3417(200009)192:1<121:FIOTFL>2.0.ZU;2-6
Abstract
Recently published studies suggest that the procoagulant receptor protein t issue factor (TF) is involved in vitro in cell adhesion and migration, via an interaction of its cytoplasmic domain with cytoskeletal proteins, Intere stingly, TF is abundantly expressed in myocardium, but not in skeletal musc le. To elucidate the possible roles of TF in the myocardium, this study exa mined the cellular distribution of TF in relation to cytoskeletal proteins, as well as its relative amounts in different segments of premature, mature , and pathologically altered cardiac muscle. In juvenile and adult hearts, TF was predominantly detectable in the transverse part of the intercalated discs, where it co-localized with cytoskeletal proteins such as desmin and vinculin, The lowest amount of TF was observed in right atrial and the high est in left ventricular myocardium, which correlated with the number of con tact sites of cardiomyocytes in these segments of the cardiac muscle. Lower levels of TF were present in structurally altered myocardium from patients with hypertension or ventricular hypertrophy. In addition, TF expression w as decreased in human heart during sepsis and transiently decreased in rabb it heart in an endotoxaemia model, which indicates that a reduction in TF m ay contribute to cardiac failure in sepsis. The microtopography of TF at ca rdiomyocyte contact sites indicates that TF may play a structural role in t he maintenance of cardiac muscle. Copyright (C) 2000 John Wiley & Sons, Ltd .