High-density lipoprotein reduces epidermal growth factor-induced DNA synthesis in vascular smooth muscle cells

Ko, Yon; Häring, Roswitha; Stiebler, Heike; Wieczorek, A; Vetter, Hans; Sachinidis, Agapios

doi:10.1016/0021-9150(93)90027-r

Cited by 25 publications

(6 citation statements)

References 15 publications

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“…In addition, the HDL-C/TC ratio was an independent predictor of diffuse atherosclerosis in multivariate analysis. These results are consistent with the anti-atherogenic effects of HDL that are related to its role in reverse cholesterol transport [14] and also to its antioxidant [15], vasodilatory [16][17][18], antiproliferative [19] and antithrombotic [16,20] properties. A low HDL-C/TC ratio has been associated with CVD [21], CAD [22,23] and PAD [24].…”

Section: Discussionsupporting

confidence: 85%

Cardiovascular risk factors associated with clinically isolated and diffuse atherosclerosis in Spanish patients with coronary artery disease

Meco

Pinto

Escribà

et al. 1998

Eur J Clin Investigation

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Section: Discussionsupporting

confidence: 85%

Cardiovascular risk factors associated with clinically isolated and diffuse atherosclerosis in Spanish patients with coronary artery disease

Meco

Pinto

Escribà

et al. 1998

Eur J Clin Investigation

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“…EGF-induced mitogenesis and contraction in arterial smooth muscle occur within a similar concentration range (10 Ϫ10 to 10 Ϫ7 mol/L). 15 Important here is the finding that the function of growth factors is significantly altered in hypertension.…”

Section: Discussionmentioning

confidence: 99%

Arterial Epidermal Growth Factor Receptor Expression in Deoxycorticosterone Acetate–Salt Hypertension

Northcott

Florian²,

Dorrance³

et al. 2001

Hypertension

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Abstract-Epidermal growth factor (EGF) causes contraction in arteries from deoxycorticosterone acetate (DOCA)-salt hypertensive rats but not in normotensive sham rats. We hypothesized that an increase in the number of EGF receptors (EGFRs) in arteries from DOCA-salt rats enables the observed contraction to EGF to occur. DOCA-salt rats had a systolic blood pressure Ͼ170 mm Hg, whereas all sham rats had a systolic blood pressure Ͻ125 mm Hg. Thoracic aorta were removed for measurement of isometric force, EGFR mRNA levels, and EGFR protein levels. EGF caused a significant contraction in endothelium-denuded aorta from DOCA-salt rats (38Ϯ7% of maximal phenylephrine-induced [10 mol/L] contraction) compared with aorta from sham rats (4Ϯ2%). The EGFR tyrosine kinase-specific inhibitors 4,5-dianilinophthalimide (10 mol/L) and AG1478 (250 nmol/L) reduced contraction in aorta from DOCA-salt by 85Ϯ14% and 65Ϯ10%, respectively. EGFR mRNA in DOCA-salt aorta was increased 4.2-fold compared with that in sham aorta. However, Western analyses of membrane-enriched and whole-tissue lysate of aorta from sham and DOCA-salt revealed no statistical difference in the density of EGFR protein between sham and DOCA-salt aorta. These data refute our hypothesis and suggest that a change downstream of EGFR is responsible for enabling EGF-induced contraction in hypertension. Key Words: EGF Ⅲ mineralocorticoid Ⅲ artery Ⅲ tyrosine kinase E pidermal growth factor (EGF) is a 6-kDa protein derived from a larger propeptide found in platelets, kidneys, and salivary glands. EGF binds 1 of 4 recognized receptorsErbB1 (EGF receptor [EGFR], Her-1), the orphan receptor ErbB2 (Neu, Her-2), ErbB3 (Her-3), and ErbB4 (Her-4)-to cause receptor dimerization and intermolecular autophosphorylation through activation of the cytoplasmic tyrosine kinase integral to these receptors. 1,2 The autophosphorylated dimer recruits adaptor proteins to lead to activation of multiple signaling pathways, including phosphoinositide 3-kinase, Janus kinase/signal transducer, and activator of transcription (Jak/STAT) and mitogen-activated protein kinase (MAPK) cascades. 3 Dimerization is necessary for receptor activation and thus physical clustering of receptors through increased expression or reorganization could potentially facilitate activation of these receptors.Growth factors such as EGF are vascular smooth muscle cell mitogens. 4 Recently, growth factors have been discovered to modulate smooth muscle contractility. 5-7 Inappropriate vascular growth or remodeling and enhanced contractility are commonly observed in forms of human and experimental hypertension. 8 We previously presented the novel finding of a significant contraction to EGF in arteries from hypertensive but not normotensive rats 9 and herein test the hypothesis that contraction to EGF is enabled in arteries of hypertensive animals because of an increased expression of the primary receptor for EGF, EGFR. It is becoming increasingly evident that the EGFR serves as a relay station for signaling of crucial vasoactive ...

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“…Novotny et al previously reported that TFPI covalently binds to apolipoprotein A‐II [24]. And also, apolipoprotein A‐II reduces EGF‐induced DNA synthesis in SMCs [25]. Therefore, it is possible that the anti‐proliferative effects of h‐rTFPI may be mediated through the interaction between h‐rTFPI and apolipoprotein A‐II, although the precise mechanism still remains unknown.…”

Section: Discussionmentioning

confidence: 99%

Human recombinant tissue‐factor pathway inhibitor prevents the proliferation of cultured human neonatal aortic smooth muscle cells

et al. 1997

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Tissue-factor pathway inhibitor (TFPI) inhibits the procoagulant activity of the tissue-factor/factor Vila complex. It was recently reported that TFPI prevented restenosis following tissue injury in a rabbit atherosclerotic model. In order to clarify the mechanism behind this successful prevention of restenosis, we investigated the direct effect of human recombinant TFPI (hrTFPI) on the proliferation of cultured human neonatal aortic smooth muscle cells (hSMC). We found that h-rTFPI exhibits inhibitory activity toward hSMC proliferation, while h-rTFPI-C which lacks the carboxyl (C)-terminal region does not. Furthermore, we found that h-rTFPI binds to hSMCs with Ä" d = 526 nM but that this binding is inhibited by the addition of the synthetic C-terminal peptide, Lys 254 -Met 276 , to h-rTFPI. Thus, the interaction of h-rTFPI with hSMCs mediated via the C-terminal region is responsible for the anti-proliferative action of h-rTFPI. On the basis of these results, we presume that the anti-proliferative effect of h-rTFPI in addition to its anticoagulant function plays a significant role in preventing restenosis following tissue injury.

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High-density lipoprotein reduces epidermal growth factor-induced DNA synthesis in vascular smooth muscle cells

Cited by 25 publications

References 15 publications

Cardiovascular risk factors associated with clinically isolated and diffuse atherosclerosis in Spanish patients with coronary artery disease

Cardiovascular risk factors associated with clinically isolated and diffuse atherosclerosis in Spanish patients with coronary artery disease

Arterial Epidermal Growth Factor Receptor Expression in Deoxycorticosterone Acetate–Salt Hypertension

Human recombinant tissue‐factor pathway inhibitor prevents the proliferation of cultured human neonatal aortic smooth muscle cells

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