17β-Estradiol Up-Regulates Vascular Endothelial Growth Factor Receptor-2 Expression in Human Myometrial Microvascular Endothelial Cells: Role of Estrogen Receptor-α and -β

Gargett, Caroline E.; Zaitseva, Marina; Bucak, Kristina; Chu, Simon; Fuller, Peter J.; Rogers, Peter A. W.

doi:10.1210/jc.2001-010588

Cited by 52 publications

(41 citation statements)

References 56 publications

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“…Our results could be interpreted by the fact that the response could vary among different subjects, or by a loss of ER expression in most samples. Gargett et al (2002) report a moderate increase in Flk-1/KDR expression in E 2 -treated myometrial endothelial cells, mediated primarily by ER . These discrepancies may reflect differences in endothelial cell origin and/or conditions of culture such as the number of passages.…”

Section: E 2 and In Vitro Regulation Of Flk-1/kdr Expression In Endotmentioning

confidence: 82%

Regulation of the vascular endothelial growth factor (VEGF) receptor Flk-1/KDR by estradiol through VEGF in uterus

Hervé¹,

Meduri²,

Petit³

et al. 2006

Journal of Endocrinology

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The induction of vascular endothelial growth factor (VEGF) expression by 17 -estradiol (E 2 ) in many target cells, including epithelial cells, fibroblasts and smooth muscle cells, suggests a role for this hormone in the modulation of angiogenesis and vascular permeability. We have already described a cyclic increase in Flk-1/KDRexpressing capillaries in the human endometrium during the proliferative and mid-secretory phases, strongly suggestive of an E 2 effect on Flk-1/KDR expression in the endometrial capillaries. However, it is unclear whether these processes are due to a direct effect of E 2 on endothelial cells. Using immunohistochemistry, we report an increase in Flk-1/KDR expression in endometrial capillaries of ovariectomized mice treated with E 2 , or both E 2 and progesterone. This process is mediated through estrogen receptor (ER) activation. In vitro experiments using quantitative RT-PCR analysis demonstrate that Flk-1/KDR expression was not regulated by E 2 in human endothelial cells from the microcirculation (HMEC-1) or macrocirculation (HUVEC), even in endothelial cells overexpressing ER or ER after ER-mediated adenovirus infection. In contrast, Flk-1/KDR expression was up-regulated by VEGF itself, in a time-and dosedependent manner, with the maximal response at 10 ng/ ml. Thus, we suggest that E 2 up-regulates Flk-1/KDR expression in vivo in endothelial cells mainly through the modulation of VEGF by a paracrine mechanism. It is currently unknown whether or not the endothelial origin might account for differences in the E 2 -modulation of VEGF receptor expression, particularly in relation to the vascular bed of sex steroid-responsive tissues.

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Section: E 2 and In Vitro Regulation Of Flk-1/kdr Expression In Endotmentioning

confidence: 82%

Regulation of the vascular endothelial growth factor (VEGF) receptor Flk-1/KDR by estradiol through VEGF in uterus

Hervé¹,

Meduri²,

Petit³

et al. 2006

Journal of Endocrinology

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“…A comparable result was described first in vascular endothelium of rat uterus by Wang et al (1999), and then in vessels of human endometrium (Critchley et al 2001), where ER␤ was the only steroid receptor expressed. Moreover, a number of studies have shown ER␣ to be important in the functioning and growth of endothelium both in vitro and in vivo, e.g., Brouchet et al (2001) and Gargett et al (2002), where estrogen tends to mediate transcription via ER␣ rather than ER␤. Therefore, estrogen incubation increased VEGFR-2 expression and VEGF binding only in ER␣-positive myometrial microvascular endothelial cells, but expression of ER␣ was low and variable among subjects (13 of 21 samples).…”

Section: Discussionmentioning

confidence: 99%

Expression of Estrogen Receptors in Human Corpus Cavernosum and Male Urethra

Dietrich

Haitel

Huber

et al. 2004

J Histochem Cytochem.

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S U M M A R Y Estrogen, largely produced in testis and adrenal gland, may play important roles in male reproduction. Most of the effects of estrogens are mediated by binding of estrogen to one or both of the two estrogen receptor (ER) subtypes ␣ and ␤ . Recently, they have been described in testis, prostate, and efferent ducts, mostly in rodents. The goal of this study was to prove the evidence of ERs in human corpus cavernosum and male urethra, exploring the protein expression of these receptors by immunohistochemistry. Corpus cavernosum and corpus spongiosum smooth muscle was immunoreactive for the androgen receptor (AR), ER ␣ , and strongly for ER ␤ . Endothelial cells were negative for AR, sporadically positive for ER ␣ , and positive for ER ␤ . Urethral epithelium showed strong nuclear expression of AR, predominantly in the basal cell layer, and nuclear expression of ER ␣ in the intermediate cells. ER ␤ was highly expressed in almost all urethral nuclei and, much more weakly, in cytoplasm. Progesterone receptor (PGR) was negative in all cases and all tissues. These results represent the first report that ER ␣ and particularly ER ␤ are regularly expressed in human penile tissue.

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“…These receptors, as has been described in non-classical sex steroidal target organs including vascular and adrenal tissue, influence the expression of a variety of genes (Gargett et al 2002, Serova et al 2002. However, one characteristic feature of the genes involved in fatty acid oxidation is their sensitivity and regulation by the peroxisomal proliferator-activated receptor (PPAR) family of transcription factors (Gulick et al 1994, Mascaro et al 1998, Wu et al 1999.…”

Section: Introductionmentioning

confidence: 99%

17beta-estradiol upregulates the expression of peroxisome proliferator-activated receptor alpha and lipid oxidative genes in skeletal muscle

Campbell

Mehan

Tunstall

et al. 2003

Journal of Molecular Endocrinology

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This study examined the actions of 17β-estradiol (E 2 ) and progesterone on the regulation of the peroxisome proliferator-activated receptors (PPARα and PPARγ) family of nuclear transcription factors and the mRNA abundance of key enzymes involved in fat oxidation, in skeletal muscle. Specifically, carnitine palmitoyltransferase I (CPT I), β-3-hydroxyacyl CoA dehydrogenase (β-HAD), and pyruvate dehydrogenase kinase 4 (PDK4) were examined. Sprague-Dawley rats were ovariectomized and treated with placebo (Ovx), E 2 , progesterone, or both hormones in combination (E+P). Additionally, sham-operated rats were treated with placebo (Sham) to serve as controls. Hormone (or vehicle only) delivery was via time release pellets inserted at the time of surgery, 15 days prior to analysis. E 2 treatment increased PPARα mRNA expression and protein content (P<0·05), compared with Ovx treatment. E 2 also resulted in upregulated mRNA of CPT I and PDK4 (P<0·05). PPARγ mRNA expression was also increased (P<0·05) by E 2 treatment, although protein content remained unaltered. These data demonstrate the novel regulation of E 2 on PPARα and genes encoding key proteins that are pivotal in regulating skeletal muscle lipid oxidative flux.

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17β-Estradiol Up-Regulates Vascular Endothelial Growth Factor Receptor-2 Expression in Human Myometrial Microvascular Endothelial Cells: Role of Estrogen Receptor-α and -β

Cited by 52 publications

References 56 publications

Regulation of the vascular endothelial growth factor (VEGF) receptor Flk-1/KDR by estradiol through VEGF in uterus

Regulation of the vascular endothelial growth factor (VEGF) receptor Flk-1/KDR by estradiol through VEGF in uterus

Expression of Estrogen Receptors in Human Corpus Cavernosum and Male Urethra

17beta-estradiol upregulates the expression of peroxisome proliferator-activated receptor alpha and lipid oxidative genes in skeletal muscle

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