Endothelin-1 and Human Platelets

Jagroop, IA; Daskalopoulou, Stella S.; Mikhailidis, Dimitri P.

doi:10.2174/157016105774329453

Cited by 32 publications

(17 citation statements)

References 95 publications

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“…We detected a modest enrichment of genes involved in ''cell-to-cell signaling and interaction'' (range, P = 4.52 3 10 À2 to 1.17 3 10 À1 , Benjamini-Hochberg corrected for multiple testing; n = 10). Notably, these genes included THBS1 (encoding thrombospondin 1), WASL (Wiskott-Aldrich syndrome-like), and EDN1 (endothelin 1), which have a marked role in the activation of blood platelets (Dorahy et al 1997;Falet et al 2002;Jagroop et al 2005). This suggests the involvement of non-cell-autonomous mechanisms for the regulation of platelet count, whereby extrinsic factors expressed by MOs or their progeny regulate the differentiation and proliferation of the hematopoietic stem cells toward MKs and the removal of senescent platelets from the circulation by liverresiding MO-derived macrophages.…”

Section: Enrichment Patterns Of Snps Associated With Closely Related mentioning

confidence: 99%

Maps of open chromatin highlight cell type–restricted patterns of regulatory sequence variation at hematological trait loci

et al. 2013

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Nearly three-quarters of the 143 genetic signals associated with platelet and erythrocyte phenotypes identified by metaanalyses of genome-wide association (GWA) studies are located at non-protein-coding regions. Here, we assessed the role of candidate regulatory variants associated with cell type-restricted, closely related hematological quantitative traits in biologically relevant hematopoietic cell types. We used formaldehyde-assisted isolation of regulatory elements followed by next-generation sequencing (FAIRE-seq) to map regions of open chromatin in three primary human blood cells of the myeloid lineage. In the precursors of platelets and erythrocytes, as well as in monocytes, we found that open chromatin signatures reflect the corresponding hematopoietic lineages of the studied cell types and associate with the cell typespecific gene expression patterns. Dependent on their signal strength, open chromatin regions showed correlation with promoter and enhancer histone marks, distance to the transcription start site, and ontology classes of nearby genes. Cell type-restricted regions of open chromatin were enriched in sequence variants associated with hematological indices. The majority (63.6%) of such candidate functional variants at platelet quantitative trait loci (QTLs) coincided with binding sites of five transcription factors key in regulating megakaryopoiesis. We experimentally tested 13 candidate regulatory variants at 10 platelet QTLs and found that 10 (76.9%) affected protein binding, suggesting that this is a frequent mechanism by which regulatory variants influence quantitative trait levels. Our findings demonstrate that combining large-scale GWA data with open chromatin profiles of relevant cell types can be a powerful means of dissecting the genetic architecture of closely related quantitative traits.

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Section: Enrichment Patterns Of Snps Associated With Closely Related mentioning

confidence: 99%

Maps of open chromatin highlight cell type–restricted patterns of regulatory sequence variation at hematological trait loci

et al. 2013

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“…However, as recently reviewed, ET-1 effects on platelets are still conflicting [328]: some studies showed that in vitro exposure to ET-1 induces platelet activation or increases platelet responses to aggregating agonists [327–329], other studies, however, failed to detect any direct effect [329] or even showed a decrease in platelet responses [328]. …”

Section: Influence Of Adipocytokines On Platelets and Vascular Smomentioning

confidence: 99%

Adipocytokines in Atherothrombosis: Focus on Platelets and Vascular Smooth Muscle Cells

Anfossi

Russo

Doronzo

et al. 2010

Mediators of Inflammation

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Visceral obesity is a relevant pathological condition closely associated with high risk of atherosclerotic vascular disease including myocardial infarction and stroke. The increased vascular risk is related also to peculiar dysfunction in the endocrine activity of adipose tissue responsible of vascular impairment (including endothelial dysfunction), prothrombotic tendency, and low-grade chronic inflammation. In particular, increased synthesis and release of different cytokines, including interleukins and tumor necrosis factor-α (TNF-α), and adipokines—such as leptin—have been reported as associated with future cardiovascular events. Since vascular cell dysfunction plays a major role in the atherothrombotic complications in central obesity, this paper aims at focusing, in particular, on the relationship between platelets and vascular smooth muscle cells, and the impaired secretory pattern of adipose tissue.

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“…52 However, the effect of ET-1 on platelets is still controversial. 53 Resveratrol, a natural polyphenolic compound extracted from plants, seems to inhibit platelet aggregation and change platelet reactivity in inflammatory processes including acute pancreatitis. 54,55 There is also some evidence that resveratrol prevents leukocyte recruitment and endothelial barrier disruption in ischemic/reperfusion injury 56 and that it upregulates nitric oxide synthase mRNA expression in endothelial cells.…”

Section: Pathophysiology Of Hemostatic Disorders In Acute Pancreatitimentioning

confidence: 99%

Coagulation, Platelets, and Acute Pancreatitis

Kakafika

Papadopoulos²,

Mimidis³

et al. 2007

Pancreas

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Acute pancreatitis generates a complex cascade of immunological events that affect the pathogenesis and the progression of this disease. Several inflammatory mediators seem to play a critical role in the pathogenesis of pancreatitis and the subsequent inflammatory response. In turn, these mediators can influence hemostasis. Coagulation abnormalities occur in acute pancreatitis and are related to its severity. The contribution of blood platelets in the disturbed hemostasis in acute pancreatitis, although extensively studied, remains obscure. This article reviews the local and systemic implications of hemostatic abnormalities during acute pancreatitis. Furthermore, we discuss the prognostic value and the potential therapeutic implications of platelet activation and other hemostatic variables.

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Endothelin-1 and Human Platelets

Cited by 32 publications

References 95 publications

Maps of open chromatin highlight cell type–restricted patterns of regulatory sequence variation at hematological trait loci

Maps of open chromatin highlight cell type–restricted patterns of regulatory sequence variation at hematological trait loci

Adipocytokines in Atherothrombosis: Focus on Platelets and Vascular Smooth Muscle Cells

Coagulation, Platelets, and Acute Pancreatitis

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