Endothelial cell dysfunction and coagulation

Vallet, B.; Wiel, É.

doi:10.1097/00003246-200107001-00015

Cited by 100 publications

(61 citation statements)

References 50 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…In the present study, in four separate experiments we observed no significant difference in LPS toxicity between Tir8Ϫ͞Ϫ and ϩ͞ϩ mice. Mononuclear phagocytes and endothelial cells, which generally do not express TIR8 (13,14), are credited with playing a central role in endotoxic shock (28,29). The apparent discrepancy between results reported here and those of Wald et al is likely due to the different genetic background and may reflect a differential involvement in the systemic toxicity of LPS of cellular components other than myelomonocytic and endothelial cells.…”

Section: Discussioncontrasting

confidence: 78%

Intestinal inflammation in mice deficient in Tir8 , an inhibitory member of the IL-1 receptor family

Garlanda

Riva

Polentarutti

et al. 2004

Proc. Natl. Acad. Sci. U.S.A.

242

247

View full text Add to dashboard Cite

TIR8, also known as single Ig IL-1-related receptor, is a member of the IL-1 receptor͞Toll-like receptor (TLR) superfamily, which acts as an intracellular decoy for components of the signaling pathway. Here we report that Tir8 has a unique pattern of expression, which includes mucosal tissues and dendritic cells (DC). Tir8-deficient DC showed increased cytokine production in response to TLR agonists (lipopolysaccharide, CpG oligodeoxynucleotides). Tir8-deficient mice had normal susceptibility to systemic lipopolysaccharide toxicity and to i.p. or s.c. inflammation. However, Tir8-deficient mice were more susceptible to intestinal inflammation. Thus, TIR8 represents a negative pathway of regulation of the IL-1 receptor͞TLR system, expressed in epithelial cells and DC, crucial for tuning inflammation in the gastrointestinal tract.

show abstract

Section: Discussioncontrasting

confidence: 78%

Intestinal inflammation in mice deficient in Tir8 , an inhibitory member of the IL-1 receptor family

Garlanda

Riva

Polentarutti

et al. 2004

Proc. Natl. Acad. Sci. U.S.A.

242

247

View full text Add to dashboard Cite

show abstract

“…Cells at passage 3 from four separate animals were each thawed and grown to passage 4, combined, and then split 1:8 before freezing with 10% dimethylsulfoxide (Sigma) for later plating at lower density as required. Note that in test studies, the data from these cells were indistinguishable from our previously published data on prepassage 4 cells (Vallet & Wiel 2001, Bird et al 2000.…”

Section: Isolation Of Uaeccontrasting

confidence: 61%

“…Endothelial cells (EC) function at many levels to maintain a balance between angiogenesis and apoptosis (Schriffin 2001), vasodilation and vasoconstriction , and coagulation and fibrinolysis (Baumgartner-Parzer & Waldhausl 2001, Vallet & Wiel 2001, Levi et al 2002. In addition, the endothelium serves as a selective permeability barrier between the blood and tissue, including the brain (Albert et al 1997), and produces a variety of growth factors and peptide hormones ( Miller 1999, Vapaatalo & Mervaala 2001.…”

Section: Introductionmentioning

confidence: 99%

Pregnancy-enhanced store-operated Ca2+ channel function in uterine artery endothelial cells is associated with enhanced agonist-specific transient receptor potential channel 3-inositol 1,4,5-trisphosphate receptor 2 interaction

Gifford¹,

Feng²,

Bird³

2006

Journal of Endocrinology

View full text Add to dashboard Cite

We have previously shown that endothelial cells (EC) derived from the uterine artery (UA) of both pregnant (P-UAEC) and nonpregnant (NP-UAEC) ewes show a biphasic intracellular free Ca 2C ([Ca 2C ] i ) response after ATP stimulation. In each case, the initial transient peak, caused by the release of Ca 2C from the intracellular Ca 2C stores, is mediated by purinergic receptor-Y2 and is very similar in both cell types. However, the sustained phase in particular, caused by the influx of extracellular Ca 2C, is heightened in the P-UAEC, and associates with an increased ability of the cells to demonstrate enhanced capacitative Ca 2C entry (CCE) via store-operated channels (SOCs). Herein we demonstrated that the difference in the sustained [Ca 2C ] i response is maintained for at least 30 min. When 2-aminoethoxydiphenyl borate (2APB) (an inhibitor of the inosital 1,4,5-trisphosphate receptor (IP3R) and possibly SOC) was used in conjunction with ATP, it was capable of completely inhibiting CCE. Since 2APB can inhibit SOC in some cell types and 2APB was capable of inhibiting CCE in the UAEC model, the role of SOC in CCE was first evaluated using the classical inhibitor La ] i response. Since canonical transient receptor potential channels (TRPCs) have recently been identified as putative SOCs in many cell types, including EC, the expression levels of several isoforms were evaluated in UAEC. Expression of TRPC3 and TRPC6 channels in particular was detected, but no significant difference in expression level was found between NP-and P-UAEC. Nonetheless, we were able to show that IP3R2 interacts with TRPC3 in UAEC, forming a protein complex, and that this interaction is considerably enhanced in an agonist sensitive manner by pregnancy. Thus, while IP3R and TRPC isoforms are not altered in their expression by pregnancy, enhanced functional interaction of TRPC3 with IP3R2 may underlie pregnancy-enhanced CCE in the UAEC model and so explain the prolonged [Ca 2C ] i sustained phase seen in response to ATP.

show abstract

“…Tissue factor triggers the extrinsic coagulation pathway, plays a key role in homeostasis and in several thrombotic diseases, and is also involved in cell signaling (4)(5)(6)(7)(8)(9)(10). Tissue factor is a glycosylated membrane protein that consists of a single polypeptide chain of 263 amino acids with an apparent molecular mass of 46 kDa, as determined by SDS-PAGE electrophoresis (5,(11)(12)(13)(14).…”

Section: The Structure and Location Of Tissue Factormentioning

confidence: 99%

Endothelial cells, tissue factor and infectious diseases

Lópes-Bezerra

Filler

2003

Braz J Med Biol Res

View full text Add to dashboard Cite

Tissue factor is a transmembrane procoagulant glycoprotein and a member of the cytokine receptor superfamily. It activates the extrinsic coagulation pathway, and induces the formation of a fibrin clot. Tissue factor is important for both normal homeostasis and the development of many thrombotic diseases. A wide variety of cells are able to synthesize and express tissue factor, including monocytes, granulocytes, platelets and endothelial cells. Tissue factor expression can be induced by cell surface components of pathogenic microorganisms, proinflammatory cytokines and membrane microparticles released from activated host cells. Tissue factor plays an important role in initiating thrombosis associated with inflammation during infection, sepsis, and organ transplant rejection. Recent findings suggest that tissue factor can also function as a receptor and thus may be important in cell signaling. The present minireview will focus on the role of tissue factor in the pathogenesis of septic shock, infectious endocarditis and invasive aspergillosis, as determined by both in vivo and in vitro models. Correspondence

show abstract

Endothelial cell dysfunction and coagulation

Cited by 100 publications

References 50 publications

Intestinal inflammation in mice deficient in Tir8 , an inhibitory member of the IL-1 receptor family

Intestinal inflammation in mice deficient in Tir8 , an inhibitory member of the IL-1 receptor family

Pregnancy-enhanced store-operated Ca2+ channel function in uterine artery endothelial cells is associated with enhanced agonist-specific transient receptor potential channel 3-inositol 1,4,5-trisphosphate receptor 2 interaction

Endothelial cells, tissue factor and infectious diseases

Contact Info

Product

Resources

About