Physiological Effects of Androgens on Human Vascular Endothelial and Smooth Muscle Cells in Culture

Nheu, Lina; Ling, Shanhong; Nazareth, Lester; Luo, Rui Zhi; Komesaroff, Paul A.

doi:10.1210/endo-meetings.2011.part1.p1.p1-2

Cited by 7 publications

(7 citation statements)

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“…As part of the investigations into the modulation exerted on pSMC phenotype by testosterone, we also evaluated the effect on cell proliferation activated after LPS challenge as we previously demonstrated. In agreement with the results of other authors (Nheu et al, 2011; Niu et al, 2001), unstimulated pSMCs displayed a higher proliferation rate in the presence of testosterone, which occurred together with an increase of p‐ERK1/2. Interestingly, testosterone eliminated the mitogenic effect of LPS on pSMCs as well as the early phosphorylation of ERK1/2.…”

Section: Discussionsupporting

confidence: 93%

Testosterone abrogates TLR4 activation in prostate smooth muscle cells contributing to the preservation of a differentiated phenotype

Leimgruber

Quintar

García

et al. 2013

Journal Cellular Physiology

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Prostate smooth muscle cells (pSMCs) are capable of responding to inflammatory stimuli by secreting proinflammatory products, which causes pSMCs to undergo dedifferentiation. Although it has been proposed that androgens decrease proinflammatory molecules in many cells and under various conditions, the role of testosterone in the prostate inflammatory microenvironment is still unclear. Therefore, our aim was to evaluate if testosterone was able to modulate the pSMCs response to bacterial LPS by stimulating primary pSMC cultures, containing testosterone or vehicle, with LPS (1 or 10 µg/ml) for 24-48 h. The LPS challenge induced pSMCs dedifferentiation as evidenced by a decrease of calponin and alpha smooth muscle actin along with an increase of vimentin in a dose-dependent manner, whereas testosterone abrogated these alterations. Additionally, an ultrastructural analysis showed that pSMCs acquired a secretory profile after LPS and developed proteinopoietic organelles, while pSMCs preincubated with testosterone maintained a more differentiated phenotype. Testosterone downregulated the expression of surface TLR4 in control cells and inhibited any increase after LPS treatment. Moreover, testosterone prevented IκB-α degradation and the LPS-induced NF-κB nuclear translocation. Testosterone also decreased TNF-α and IL6 production by pSMCs after LPS as quantified by ELISA. Finally, we observed that testosterone inhibited the induction of pSMCs proliferation incited by LPS. Taken together, these results indicate that testosterone reduced the proinflammatory pSMCs response to LPS, with these cells being less reactive in the presence of androgens. In this context, testosterone might have a homeostatic role by contributing to preserve a contractile phenotype on pSMCs under inflammatory conditions.

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Section: Discussionsupporting

confidence: 93%

Testosterone abrogates TLR4 activation in prostate smooth muscle cells contributing to the preservation of a differentiated phenotype

Leimgruber

Quintar

García

et al. 2013

Journal Cellular Physiology

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“…Plasma levels of DHEA decline linearly with age in both males and females, and this age-related decline is known to be independently associated with cardiovascular mortality [28]. Consistent with this observation, DHEA is known to have an anti-atherosclerotic effect through its inhibition of proliferation and migration of vascular smooth muscle cells [11] and its protective effect against superoxide injury on endothelial cells [29]. DHEA stimulates NO release in cultured human endothelial cells and increases aortic endothelial nitric oxide synthase (eNOS) in ovariectomized Wistar rats [30].…”

Section: Discussionmentioning

confidence: 78%

Dehydroepiandrosterone prevents linoleic acid-induced endothelial cell senescence by increasing autophagy

et al. 2015

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“…Androgens are thought to modulate phenotypic changes of VSMCs through the upregulation of proliferation and interactions with intracellular signaling pathways induced by proinflammatory cytokines 64,65) . Several studies have revealed that androgens enhance tumor necrosis factor and vascular cell adhesion molecule-1 expressions through interaction between the AR and nuclear factor-kappa B signaling pathway [66][67][68] . Androgens also inhibit the production of interleukin 6, interleukin 1 beta, and expression of the intracellular adhesion molecule-1 and monocyte chemoattractant protein-1 in various cell types 69,70) .…”

Section: Ar Plays a Pivotal Role In Vegf-stimulated Akt And Enos Signmentioning

confidence: 99%

Roles of the Androgen – Androgen Receptor System in Vascular Angiogenesis

Yoshida

Ikeda

Aihara

2016

JAT

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Although many clinical studies have shown that a low testosterone level is associated with cardiovascular diseases, the role of androgens in cardiovascular physiology and pathophysiology remains controversial. Androgens exert various actions in their target organs, and the androgen receptor (AR) is widely distributed in several tissues, including endothelial cells, smooth muscle cells, and fibroblasts, in the vascular system. Biological activities of androgens are predominantly mediated through the AR by the transcriptional control of target genes and interaction with multiple signaling pathways. To clarify the molecular mechanisms of androgens in cardiovascular disease, we examined a pathological model using AR knockout mice and showed that the androgen -AR system has protective effects on cardiovascular remodeling against cardiovascular stress. In this review, we focus on the role of the androgen -AR system in angiogenesis after ischemic stress.

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Physiological Effects of Androgens on Human Vascular Endothelial and Smooth Muscle Cells in Culture

Cited by 7 publications

References 0 publications

Testosterone abrogates TLR4 activation in prostate smooth muscle cells contributing to the preservation of a differentiated phenotype

Testosterone abrogates TLR4 activation in prostate smooth muscle cells contributing to the preservation of a differentiated phenotype

Dehydroepiandrosterone prevents linoleic acid-induced endothelial cell senescence by increasing autophagy

Roles of the Androgen – Androgen Receptor System in Vascular Angiogenesis

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