Effect of platelet factors on migration of cultured bovine aortic endothelial and smooth muscle cells.

Bell, Leonard; Madri, Joseph A.

doi:10.1161/01.res.65.4.1057

Cited by 110 publications

(48 citation statements)

References 30 publications

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“…A developmental role of 5-HT has been described previously in non-neural tissues as diverse as the palate and craniofacial mesenchyme (Zimmerman et al, 1983;Shuey et al, 1992;Moiseiwitch and Lauder, 1995), the heart (Yavarone et al, 1993;Choi et al, 1997), and the endothelium and vascular smooth muscle (Bottaro et al, 1985;Bell and Madri, 1989;Tamura et al, 1997). cell migration, typically mediated by 5-HT 2 receptor subtypes, has been reliably documented in all these instances (Zimmerman et al, 1983;Bottaro et al, 1985;Bell and Madri, 1989;Shuey et al, 1992;Yavarone et al, 1993;Moiseiwitch and Lauder, 1995;Choi et al, 1997;Tamura et al, 1997).…”

Section: Possible Mechanisms Of Serotonin-induced Alterations In 5-htmentioning

confidence: 79%

“…cell migration, typically mediated by 5-HT 2 receptor subtypes, has been reliably documented in all these instances (Zimmerman et al, 1983;Bottaro et al, 1985;Bell and Madri, 1989;Shuey et al, 1992;Yavarone et al, 1993;Moiseiwitch and Lauder, 1995;Choi et al, 1997;Tamura et al, 1997). The involvement of 5-HT in regulating cell migration may be more widespread than anticipated, given the broad distribution of transient 5-HTT immunoreactivity recently described in mouse embryos (Hansson et al, 1999).…”

Section: Possible Mechanisms Of Serotonin-induced Alterations In 5-htmentioning

confidence: 96%

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Barrel Pattern Formation Requires Serotonin Uptake by Thalamocortical Afferents, and Not Vesicular Monoamine Release

et al. 2001

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Thalamocortical neurons innervating the barrel cortex in neonatal rodents transiently store serotonin (5-HT) in synaptic vesicles by expressing the plasma membrane serotonin transporter (5-HTT) and the vesicular monoamine transporter (VMAT2). 5-HTT knock-out (ko) mice reveal a nearly complete absence of 5-HT in the cerebral cortex by immunohistochemistry, and of barrels, both at P7 and adulthood. Quantitative electron microscopy reveals that 5-HTT ko affects neither the density of synapses nor the length of synaptic contacts in layer IV. VMAT2 ko mice, completely lacking activity-dependent vesicular release of monoamines including 5-HT, also show a complete lack of 5-HT in the cortex but display largely normal barrel fields, despite sometimes markedly reduced postnatal growth. Transient 5-HTT expression is thus required for barrel pattern formation, whereas activity-dependent vesicular 5-HT release is not.

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Section: Possible Mechanisms Of Serotonin-induced Alterations In 5-htmentioning

confidence: 79%

Section: Possible Mechanisms Of Serotonin-induced Alterations In 5-htmentioning

confidence: 96%

Barrel Pattern Formation Requires Serotonin Uptake by Thalamocortical Afferents, and Not Vesicular Monoamine Release

et al. 2001

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“…37 Proliferation and migration of the VECs can also be strongly inhibited by TGF-β. 38,39 Apoptosis of the VECs is a major determinant of plaque erosion and thrombosis formation, which is a trigger of MI. 40 MiR-125b can regulate apoptosis by targeting transcripts encoding Mcl-1, 41 Bcl-w, 41 IL-6R, 41 and the expression of ≈14 genes inP53 network.…”

Section: Discussionmentioning

confidence: 99%

Circulating MicroRNAs and the Occurrence of Acute Myocardial Infarction in Chinese Populations

Huang

Lü

et al. 2014

Circ Cardiovasc Genet

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A cute myocardial infarction (AMI) is a leading cause of morbidity and mortality worldwide. 1 Multiple conventional risk factors and serum atherosclerotic biomarkers have been established for coronary heart disease (CHD). 2 However, advances in genomics and proteomics, especially gene-expression profiling using microarray and quantitative real-time polymerase chain reaction (qPCR), have promoted the generation of many novel molecular biomarkers for AMI with potential clinical values. 3,4 Recently, microRNAs (miRNAs) have attracted extensive interest in the field of cardiovascular diseases. 5 Clinical Perspective on p 198MiRNAs are short, endogenous, noncoding RNAs that regulate gene expressions at the posttranscriptional level by binding to the 3′-untranslated regions of their target mRNAs. 6,7 MiRNAs have now emerged as key regulators of cardiac growth, vascular development, and angiogenesis. 8,9 Recent studies demonstrated that miRNAs can be detected in circulating blood and may be useful as disease biomarkers. 10,11 The levels and identities of circulating miRNAs in cardiovascular diseases have been evaluated in a series of studies. For instance, levels of some vascular and inflammation-associated miRNAs were found to be significantly lower in the plasma of 67 patients with CHD when compared with controls, 12 and the cardiac-specific miRNA, miR-208a, was only detectable in 33 patients with AMI and not Background-Circulating microRNAs ( miRNAs) are emerging as novel disease biomarkers. We aimed to explore the association between circulating miRNAs and the occurrence of acute myocardial infarction (AMI) in Chinese populations. Methods and Results-In the discovery stage, the plasma of 20 patients with AMI and 20 controls were pooled respectively and profiled by massively parallel sequencing. Seventy-seven miRNAs showed differential expression. Selected miRNAs were validated in 178 patients with AMI and 198 controls using quantitative reverse transcriptase polymerase chain reaction assays and further replicated in 150 patients with AMI and 150 controls. Results suggest that miR-320b and miR-125b levels were significantly lower in patients with AMI than in controls in both validation populations (P<0.0001). Lower levels of miR-320b and miR-125b were associated with increased occurrence of AMI (adjusted odds ratio, 4.71; 95% confidence interval, 2.96-7.48 and odds ratio, 4.27; 95% confidence interval, 2.84-6.41, respectively). Addition of the 2 miRNAs to traditional risk factors led to a significant improvement in the area under the curve from 0.822 (95% confidence interval, 0.787-0.856) to 0.871 (95% confidence interval, 0.842-0.900), with a net reclassification improvement of 20.45% (P<0.0001) and an integrated discrimination improvement of 0.16 (P<0.0001) for patients with AMI. A functional study showed that miR-320b and miR-125b could regulate the expression profiles of genes enriched in several signal transduction pathways critical for coronary heart disease in human vascular endothelial cells. Conclusions-The...

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“…In addition to histamine from circulating blood and vascular endothelial cells, histamine can be released locally from subendothelial mast cells [1][2][3] and adventitial mast cells 4,5 in coronary arteries. Moreover, histamine can also derive from activated platelets, 6 T lymphocytes, and monocytes/macrophages. 7 By occupying H 1 receptors on endothelial cells, histamine activates endothelial nitric oxide synthase (eNOS).…”

mentioning

confidence: 99%

“…For example, histamine enhances the expression of adhesion molecules in vascular endothelial cells, thereby augmenting leukocyte-endothelial cell interactions, [11][12][13] an important onset event in atherogenesis. Histamine has also been shown to increase smooth muscle cell proliferation and migration, 6 and it has been implicated in intimal thickening and atherogenesis. 14,15 In animal models, antihistamines provided protection against intimal thickening and the development of atherosclerosis.…”

mentioning

confidence: 99%

Histamine Upregulates Gene Expression of Endothelial Nitric Oxide Synthase in Human Vascular Endothelial Cells

Burkhardt

Heinrich

et al. 2003

Circulation

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Background-Histamine has a short-term, transient, stimulating effect on endothelial nitric oxide synthase (eNOS) activity; however, long-term effects on eNOS have not been described yet. In addition, the vascular effect of histamine seems to depend critically on eNOS functionality. Therefore, we studied the effects of histamine on eNOS gene expression and function. Methods and Results-In human umbilical vein endothelial cells (HUVECs) and HUVEC-derived EA.hy 926 cells, histamine upregulated eNOS mRNA (RNase protection assay) and protein (electron microscopic immunocytochemistry) expression. The upregulation of eNOS could be prevented by mepyramine, a selective antagonist at the H 1 receptor, but not by H 2 and H 3 receptor antagonists. Incubation of EA.hy 926 cells with histamine led to the activation of calcium/calmodulin-dependent protein kinase II (CaMK II; in vitro phosphorylation assay). The histamine-induced eNOS expression was completely prevented by KN-93, an inhibitor of CaMK II. Histamine increased the activity of a 1.6-kb human eNOS promoter fragment (luciferase reporter gene assay), an effect that was also blocked by mepyramine. Under normal conditions, eNOS upregulation by histamine resulted in increased nitric oxide production (measured by nitric oxide chemiluminescence and RFL-6 reporter cell assay). Under conditions of oxidative stress, however, the eNOS upregulated by histamine produced reactive oxygen species (CM-H 2 DCFDA oxidation-based fluorescence assay). Conclusions-Stimulation of the H 1 receptor increases eNOS transcription in endothelial cells by a signaling pathway involving CaMK II. This eNOS upregulation may be protective under normal conditions, but it may become harmful under conditions of oxidative stress when eNOS produces reactive oxygen species at the expense of nitric oxide.

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Effect of platelet factors on migration of cultured bovine aortic endothelial and smooth muscle cells.

Cited by 110 publications

References 30 publications

Barrel Pattern Formation Requires Serotonin Uptake by Thalamocortical Afferents, and Not Vesicular Monoamine Release

Barrel Pattern Formation Requires Serotonin Uptake by Thalamocortical Afferents, and Not Vesicular Monoamine Release

Circulating MicroRNAs and the Occurrence of Acute Myocardial Infarction in Chinese Populations

Histamine Upregulates Gene Expression of Endothelial Nitric Oxide Synthase in Human Vascular Endothelial Cells

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