Dehydroepiandrosterone Stimulates Endothelial Proliferation and Angiogenesis through Extracellular Signal-Regulated Kinase 1/2-Mediated Mechanisms

Liu, Dongmin; Iruthayanathan, Mary; Homan, Laurie L.; Wang, Yiqiang; Yang, Lingling; Wang, Yao; Dillon, Joseph S.

doi:10.1210/en.2007-1125

Cited by 84 publications

(52 citation statements)

References 89 publications

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“…The activation of androgen receptors, expressed in both the endothelial (Yu et al 2007) and smooth muscle (Ma et al 2005) cells, regulates cell signaling pathways. However, the vascular effects of male sex hormones have also been reported to be independent of androgen receptor activation (Liu et al 2008) and to interact with intracellular calcium regulatory mechanisms, as reported for other sex steroids hormones (Zhang et al 2006).…”

Section: Discussionmentioning

confidence: 82%

Orchidectomy increases the formation of non-endothelial thromboxane A2 and modulates its role in the electrical field stimulation-induced response in rat mesenteric artery

Campo¹,

Sagredo²,

Aras-López³

et al. 2008

Journal of Endocrinology

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The aim of this study was to analyze whether endogenous male sex hormones influence the release of thromboxane A 2 (TXA 2 ) and its role in the electrical field stimulation (EFS)-induced response, as well as the mechanism involved. For this purpose, endothelium-denuded mesenteric arteries from control and orchidectomized male Sprague-Dawley rats were used to measure TXA 2 release; EFS-induced response, nitric oxide (NO), norepinephrine (NA), and prostaglandin (PG) I 2 release were also measured in the presence of the TXA 2 synthesis inhibitor furegrelate. Orchidectomy increased basal and EFS-induced TXA 2 release. Furegrelate decreased the EFS-induced contraction in arteries from control rats, but did not modify it in arteries from orchidectomized rats. The EFS-induced neuronal NO release and vasodilator response were increased by furegrelate in arteries from control rats, but were not modified in arteries from orchidectomized rats. Furegrelate did not modify the EFS-induced NA release or vasoconstrictor response in arteries from either control or orchidectomized rats. The EFS-induced PGI 2 release was not modified by furegrelate in arteries from control rats, but was increased in arteries from orchidectomized rats. The results of the present study show that endogenous male sex hormone deprivation i) increases non-endothelial TXA 2 release and ii) regulates the effect of endogenous TXA 2 on the EFS-induced response through different mechanisms that, at the least, involve the NO and PGI 2 systems. In arteries from control rats, inhibition of TXA 2 formation decreases the EFS-induced response by increasing neuronal NO release. In arteries from orchidectomized rats, the EFS-induced response is unaltered after the inhibition of TXA 2 formation, by increasing PGI 2 release.

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Section: Discussionmentioning

confidence: 82%

Orchidectomy increases the formation of non-endothelial thromboxane A2 and modulates its role in the electrical field stimulation-induced response in rat mesenteric artery

Campo¹,

Sagredo²,

Aras-López³

et al. 2008

Journal of Endocrinology

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“…Angiogenesis is a complex process with EC cell proliferation, migration, and tubulogenesis playing an essential role in ultimate new blood vessel formation [15] Corneal angiogenesis causes vascularization of avascular cornea that can lead to the decline of vision and even blindness. The pathogenesis of corneal neovascularization is still not fully understood, but it is stimulated by various growth factors, notably VEGF and bFGF that are secreted in response to hypoxia, chemical burn, chronic inflammation, infection, and trauma [22].…”

Section: Discussionmentioning

confidence: 99%

“…On the outer surface of the culture wells facing the scratches, ink lines were made perpendicular to the inside scratch and the width of the scratches at the crossing site were photographed before and after the 24 h of incubation. The cell migration rates were calculated as previously described [15].…”

Section: Cell Migration Assaymentioning

confidence: 99%

Phytochemical Isoliquiritigenin Inhibits Angiogenesis Ex Vivo and Corneal Neovascularization in Mice

Yang¹,

He²,

Qu³

et al. 2014

Altern Integr Med

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Neovascularization is often involved in many diseases and there is no effective treatment for this pathological process. In searching for potential therapies for neovascularization, we screened nineteen pre-selected small molecules isolated from herbal extracts for their possible anti-angiogenic effect in vitro and in vivo. We found that isoliquiritigenin, a chalconoid compound isolated from Chinese herb medicine licorice, potently inhibited vascular endothelial cell (EC) proliferation, migration, tube -like structure formation ex vivo. Western blot analysis shows that exposure of ECs to isoliquiritigenin inhibited extracellular signal-regulated kinase 1/2 (ERK1/2) phosphorylation. In Matrigel plug assay, isoliquiritigenin effectively blocked fibroblast growth factor-induced in vivo angiogenesis in mice. Consistently, topical application of isoliquiritigenin significantly inhibited chemical injury-induced corneal neovascularization in mice. Collectively, these results suggest that isoliquiritigenin may be a low-cost and effective natural agent to treat angiogenesis-dependent diseases.

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“…This suggests that DHEA may activate ERα by a mechanism other than direct binding and/or that cell-specific factors mitigate whether DHEA activates ER action. One possibility is that DHEA may activate MAPK that phosphorylates and activates ERα independent of ligand, a possibility that fits with DHEA activation of PM-associated intracellular MAPK signaling in endothelial cells (ECs) (Liu & Dillon 2004, Liu et al 2008.…”

Section: Dhea Activation Of Steroid Receptorsmentioning

confidence: 99%

Novel mechanisms for DHEA action

Prough

Clark

Klinge

2016

Journal of Molecular Endocrinology

134

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Dehydroepiandrosterone (3β-hydroxy-5-androsten-17-one, DHEA), secreted by the adrenal cortex, gastrointestinal tract, gonads, and brain, and its sulfated metabolite DHEA-S are the most abundant endogeneous circulating steroid hormones. DHEA actions are classically associated with age-related changes in cardiovascular tissues, female fertility, metabolism, and neuronal/CNS functions. Early work on DHEA action focused on the metabolism to more potent sex hormones, testosterone and estradiol, and the subsequent effect on the activation of the androgen and estrogen steroid receptors. However, it is now clear that DHEA and DHEA-S act directly as ligands for many hepatic nuclear receptors and G-protein-coupled receptors. In addition, it can function to mediate acute cell signaling pathways. This review summarizes the molecular mechanisms by which DHEA acts in cells and animal models with a focus on the 'novel' and physiological modes of DHEA action.

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Dehydroepiandrosterone Stimulates Endothelial Proliferation and Angiogenesis through Extracellular Signal-Regulated Kinase 1/2-Mediated Mechanisms

Cited by 84 publications

References 89 publications

Orchidectomy increases the formation of non-endothelial thromboxane A2 and modulates its role in the electrical field stimulation-induced response in rat mesenteric artery

Orchidectomy increases the formation of non-endothelial thromboxane A2 and modulates its role in the electrical field stimulation-induced response in rat mesenteric artery

Phytochemical Isoliquiritigenin Inhibits Angiogenesis Ex Vivo and Corneal Neovascularization in Mice

Novel mechanisms for DHEA action

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