Publications
111 results found
Birdsey GM, Dryden NH, Amsellem V, et al., 2008, Transcription factor Erg regulates angiogenesis and endothelial apoptosis through VE-cadherin, BLOOD, Vol: 111, Pages: 3498-3506, ISSN: 0006-4971
- Author Web Link
- Cite
- Citations: 195
Randi AM, Birdsey G, Dryden N, et al., 2008, The transcription factor Erg regulates angiogenesis and endothelial apoptosis, FASEB JOURNAL, Vol: 22, ISSN: 0892-6638
Randi AM, Amsellem V, Dryden N, et al., 2008, The adhesion molecule ICAM-2 regulates contact inhibition in endothelial cells, FASEB JOURNAL, Vol: 22, ISSN: 0892-6638
Ali F, Hamdulay SS, Kinderlerer AR, et al., 2007, Statin-mediated cytoprotection of human vascular endothelial cells: a role for Kruppel-like factor 2-dependent induction of heme oxygenase-1, J Thrombosis & Haemostasis, Vol: 5, Pages: 2537-2546
Dejana E, Taddei A, Randi AM, 2007, Foxs and Ets in the transcriptional regulation of endothelial cell differentiation and angiogenesis., Biochimica et Biophysica Acta (BBA) - Reviews on Cancer, Vol: Volume 1775, Pages: 298-312
Day JRS, Taylor KM, Lidington EA, et al., 2006, Aprotinin inhibits proinflammatory activation of endothelial cells by thrombin through the protease-activated receptor 1, JOURNAL OF THORACIC AND CARDIOVASCULAR SURGERY, Vol: 131, Pages: 21-27, ISSN: 0022-5223
- Author Web Link
- Cite
- Citations: 26
Garonna E, Birdsey GM, Botham KM, et al., 2006, Leptin-memated proliferation and migration of human endothelial depends on cyclooxygenase-2 [COX-2] activity and requires activation of vascular endothelial growth factor receptor 2 [VEGFR2], 24th Conference of the European-Society-for-Microcirculation, Publisher: KARGER, Pages: 58-58, ISSN: 1018-1172
Huang MT, Mason JC, Birdsey GM, et al., 2005, Endothelial intercellular adhesion molecule (ICAM)-2 regulates angiogenesis, BLOOD, Vol: 106, Pages: 1636-1643, ISSN: 0006-4971
- Author Web Link
- Cite
- Citations: 65
Wibaut-Berlaimont V, Randi AM, Mandryko V, et al., 2005, Atorvastatin affects leukocyte gene expression in dyslipidernia patients:: <i>in vivo</i> regulation of hemostasis, inflammation and apoptosis, JOURNAL OF THROMBOSIS AND HAEMOSTASIS, Vol: 3, Pages: 677-685, ISSN: 1538-7933
- Author Web Link
- Cite
- Citations: 34
Huang MT, Mason JC, Gerwin N, et al., 2005, Intercellular adhesion molecule (ICAM)-2 mediates angiogenesis via homophilic interaction, Experimental Biology 2005 Meeting/35th International Congress of Physiological Sciences, Publisher: FEDERATION AMER SOC EXP BIOL, Pages: A1714-A1714, ISSN: 0892-6638
Day JRS, Punjabi PP, Randi AM, et al., 2004, Clinical inhibition of the seven-transmembrane thrombin receptor (PAR1) by intravenous aprotinin during cardiothoracic surgery, CIRCULATION, Vol: 110, Pages: 2597-2600, ISSN: 0009-7322
- Author Web Link
- Cite
- Citations: 52
Randi AM, Biguzzi E, Falciani F, et al., 2003, Identification of differentially expressed genes in coronary atherosclerotic plaques from patients with stable or unstable angina by cDNA array analysis, JOURNAL OF THROMBOSIS AND HAEMOSTASIS, Vol: 1, Pages: 829-835, ISSN: 1538-7933
- Author Web Link
- Cite
- Citations: 45
Berlaimont V, Mandryko V, Haskard D, et al., 2002, Pharmacogenomics in clinical blood samples: The statin pilot study, American-Heart-Association Abstracts From Scientific Sessions, Publisher: LIPPINCOTT WILLIAMS & WILKINS, Pages: 302-302, ISSN: 0009-7322
- Author Web Link
- Cite
- Citations: 2
Mason JC, Ahmed Z, Mankoff R, et al., 2002, Statin-induced expression of decay-accelerating factor protects vascular endothelium against complement-mediated injury, CIRCULATION RESEARCH, Vol: 91, Pages: 696-703, ISSN: 0009-7330
- Author Web Link
- Cite
- Citations: 77
Thompson PW, Randi AM, Ridley AJ, 2002, Intercellular adhesion molecule (ICAM)-1, but not ICAM-2, activates RhoA and stimulates c-fos and rhoA transcription in endothelial cells., J Immunol, Vol: 169, Pages: 1007-1013, ISSN: 0022-1767
ICAM-1 and -2 are integrin-binding Ig superfamily adhesion molecules that are important for leukocyte transmigration across endothelial monolayers. ICAM-1 cross-linking is known to activate the small GTPase RhoA and induce stress fiber formation in endothelial cells, but ICAM-2 signaling has not been investigated. In this study, we compare ICAM-1 and ICAM-2 signaling and localization in HUVECs. Although ICAM-1 and ICAM-2 both localize with the actin-binding protein moesin in apical microvilli, only ICAM-1 colocalizes with moesin after cross-linking. Unlike ICAM-1, ICAM-2 does not activate RhoA or alter actin cytoskeletal organization. Interestingly, ICAM-1 stimulates transcription of c-fos, a known early response gene. In addition, it up-regulates rhoA expression, suggesting that it activates a positive feedback pathway after RhoA activation. These results indicate that in endothelial cells, ICAM-1, but not ICAM-2, rapidly stimulates signaling responses involving RhoA.
Mason JC, Ahmed Z, Lidington EA, et al., 2002, STATIN-INDUCED EXPRESSION OF COMPLEMENT INHIBITORY PROTEINS PROTECTS VASCULAR ENDOTHELIUM AGAINST COMPLEMENT-MEDIATED INJURY, RHEUMATOLOGY, Vol: 41, Pages: 8-8, ISSN: 1462-0324
McLaughlin F, Ludbrook VJ, Cox J, et al., 2001, Combined genomic and antisense analysis reveals that the transcription factor Erg is implicated in endothelial cell differentiation., Blood, Vol: 98, Pages: 3332-3339, ISSN: 0006-4971
It has recently been shown that the transcription factor Erg, an Ets family member, drives constitutive expression of the intercellular adhesion molecule 2 (ICAM-2) in human umbilical vein endothelial cells (HUVECs) and that its expression is down-regulated by the pleiotropic cytokine tumor necrosis factor alpha (TNF-alpha). To identify other Erg target genes and to define its function in the endothelium, a combined approach of antisense oligonucleotides (GeneBloc) and differential gene expression was used. Treatment of HUVECs with Erg-specific GeneBloc for 24, 48, and 72 hours suppressed Erg mRNA and protein levels at all time points. Total RNA extracted from HUVECs treated with Erg-specific or control GeneBloc was analyzed for differences in gene expression using high-density, sequence-verified cDNA arrays containing 482 relevant genes. Inhibition of Erg expression resulted in decreased expression of ICAM-2, as predicted. Four more genes decreased in Erg-deficient HUVECs were the extracellular matrix proteins SPARC and thrombospondin, the adhesive glycoprotein von Willebrand factor, and the small GTPase RhoA. Each of these molecules has been directly or indirectly linked to angiogenesis because of its role in vascular remodeling, adhesion, or shape change. Therefore, the role of Erg in vascular remodeling was tested in an in vitro model, and the results showed that HUVECs treated with Erg GeneBloc had a decreased ability to form tubulelike structures when grown on Matrigel. These results suggest that Erg may be a mediator of the TNF-alpha effects on angiogenesis in vivo.
Mason JC, Ahmed Z, Randi A, et al., 2001, Atorvastatin protects vascular endothelium against complement-mediated injury through upregulation of membrane bound complement inhibitory proteins, ARTHRITIS AND RHEUMATISM, Vol: 44, Pages: S396-S396, ISSN: 0004-3591
McDowall A, Leitinger B, Stanley P, et al., 1998, The I domain of integrin leukocyte function-associated antigen-1 is involved in a conformational change leading to high affinity binding to ligand intercellular adhesion molecule 1 (ICAM-1), JOURNAL OF BIOLOGICAL CHEMISTRY, Vol: 273, Pages: 27396-27403, ISSN: 0021-9258
- Author Web Link
- Cite
- Citations: 88
RANDI AM, HOGG N, 1994, I-DOMAIN OF BETA(2) INTEGRIN LYMPHOCYTE FUNCTION-ASSOCIATED ANTIGEN-1 CONTAINS A BINDING-SITE FOR LIGAND INTERCELLULAR-ADHESION MOLECULE-1, JOURNAL OF BIOLOGICAL CHEMISTRY, Vol: 269, Pages: 12395-12398, ISSN: 0021-9258
- Author Web Link
- Cite
- Citations: 143
RANDI AM, HOGG N, 1993, EXPRESSION AND FUNCTIONAL-PROPERTIES OF ISOLATED LFA-1 A DOMAIN, BLOOD, Vol: 82, Pages: A238-A238, ISSN: 0006-4971
This data is extracted from the Web of Science and reproduced under a licence from Thomson Reuters. You may not copy or re-distribute this data in whole or in part without the written consent of the Science business of Thomson Reuters.