Estrogen Sulfotransferase/SULT1E1 Promotes Human Adipogenesis

Ihunnah, Chibueze A.; Wada, Taira; Philips, Barbara J.; Ravuri, Sudheer; Gibbs, Robert G.; Kirisci, Levent; Rubin, J. Peter; Marra, Kacey G.; Xie, Wen

doi:10.1128/mcb.01147-13

Cited by 49 publications

(53 citation statements)

References 40 publications

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“…(Wada et al, 2011) In humans, EST expression initially was detected in subcutaneous adipose tissue from obese men and women and subsequently in adipose tissue from non-obese women, as well. (Ahima et al, 2011; Ihunnah et al, 2014) In striking contrast to pre-clinical findings, EST overexpression in human adipose tissue stem cells promoted adipocyte differentiation in association with increased expression of lipogenic genes, whereas differentiation was inhibited by EST knockdown. Further, these effects were shown to be ER-dependent, indicating that they were conferred specifically through the enzymatic activity of EST that leads to inactivation of estradiol.…”

Section: Adipose-specific Mechanisms Of Estrogen-mediated Body Weightmentioning

confidence: 80%

Estrogens and Body Weight Regulation in Men

Rubinow

2017

Advances in Experimental Medicine and Biology

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Our understanding of the metabolic roles of sex steroids in men has evolved substantially over recent decades. Whereas testosterone once was believed to contribute to metabolic risk in men, the importance of adequate androgen exposure for the maintenance of metabolic health has been demonstrated unequivocally. A growing body of evidence now also supports a critical role for estrogens in metabolic regulation in men. Recent data from clinical intervention studies indicate that estradiol may be a stronger determinant of adiposity than testosterone in men, and even short-term estradiol deprivation contributes to fat mass accrual. The following chapter will outline findings to date regarding the mechanisms whereby estrogens contribute to the regulation of body weight and adiposity in men. It will present emergent clinical data as well as preclinical findings that reveal mechanistic insights into estrogen-mediated regulation of body composition. Findings in both males and females will be reviewed, to draw comparisons and to highlight knowledge gaps regarding estrogen action specifically in males. Finally, the clinical relevance of estrogen exposure in men will be discussed, particularly in the context of a rising global prevalence of obesity and expanding clinical use of sex steroid-based therapies in men.

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Section: Adipose-specific Mechanisms Of Estrogen-mediated Body Weightmentioning

confidence: 80%

Estrogens and Body Weight Regulation in Men

Rubinow

2017

Advances in Experimental Medicine and Biology

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“…Similar to BMSCs, ASCs have the property to differentiate into osteoblastic, chondrocytic, adipocytic and neurogenic cells [38][39][40]. The influence of estrogen on differentiation of ASCs has been demonstrated earlier but remains controversial [41,42]. This may be based on the different origin of isolated cells and different setting researchers used, i.e.…”

Section: Discussionmentioning

confidence: 96%

Estrogen Receptor α and β in Mouse: Adipose-Derived Stem Cell Proliferation, Migration, and Brown Adipogenesis In Vitro

Zhang

Schmull

et al. 2016

Cell Physiol Biochem

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Background/Aims: Adipose-derived stem cells (ASCs) belong to mesenchymal stem cells and may play a potential role as seeding cells in stem cell transplantation. To be able to exploit stem cells as therapeutic tool, their defects in some important cellular functions, such as low survival rate and cellular activity, should be considered. This is especially the case for stem cells that are intended for transplantation. Of note, stem cell responses to hormones should be considered since estrogen is known to play a critical role in stem cell behavior. However, different impacts of the estrogen receptor (ER) types α and β have not been fully determined in ASC function. In this study, we investigated effects of ERα and ERβ on ASC proliferation, migration, as well as in adipogenesis. Methods: ASCs obtained from mice were cultured with 100nM ERα or ERβ agonist PPT and DPN, respectively. The ERα and ERβ antagonist ICI 182,780 (100nM) was used as control. Results: Compared to ERβ, ERα appears more potent in improving ASC proliferation and migration. Investigation of adipogenesis revealed that ERβ played a significant role in suppressing ASC-mediated brown tissue adipogenesis which is in contrast to ERα. These results correlated with reduced mRNA expression of UCP-1, PGC-1α and PPAR-γ. Conclusions: ERα plays a more critical role in promoting ASC proliferation and migration while ERβ is more potent in suppressing ASC brown adipose tissue differentiation mediated by decreased UCP-1, PGC-1α and PPAR-γ expression.

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“…After 2 hours, MA (10 mM) or RU486 (10 mM) in a-MEM containing 0.2% FBS was added on the lower side of the Transwell membrane plates for [16][17][18][19][20] hours. The migrated cells remaining in the Transwell membrane were fixed with ice-cold methanol for 20 minutes.…”

Section: Cell Migration Assaymentioning

confidence: 99%

“…Because progesterone and estrogen are critical for the growth and proliferation of breast cells during normal development and in the progression of breast cancer [16][17][18], we hypothesized that these hormones might stimulate the proliferation and differentiation of ASCs. However, estrogen derivatives did not affect ASC proliferation in a preliminary study.…”

Section: Introductionmentioning

confidence: 99%

Megestrol Acetate Increases the Proliferation, Migration, and Adipogenic Differentiation of Adipose-Derived Stem Cells via Glucocorticoid Receptor

Sung

Jeong

et al. 2015

Stem Cells Translational Medicine

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Because adipose-derived stem cells (ASCs) are usually expanded to acquire large numbers of cells for therapeutic applications, it is important to increase the production yield and regenerative potential during expansion. Therefore, a tremendous need exists for alternative ASC stimuli during cultivation to increase the proliferation and adipogenic differentiation of ASCs. The present study primarily investigated the involvement of megestrol acetate (MA), a progesterone analog, in the stimulation of ASCs, and identifies the target receptors underlying stimulation. Mitogenic and adipogenic effects of MA were investigated in vitro, and pharmacological inhibition and small interfering (si) RNA techniques were used to identify the molecular mechanisms involved in the MA-induced stimulation of ASCs. MA significantly increased the proliferation, migration, and adipogenic differentiation of ASCs in a dose-dependent manner. Glucocorticoid receptor (GR) is highly expressed compared with other nuclear receptors in ASCs, and this receptor is phosphorylated after MA treatment. MA also upregulated genes downstream of GR in ASCs, including ANGPTL4, DUSP1, ERRF11, FKBP5, GLUL, and TSC22D3. RU486, a pharmacological inhibitor of GR, and transfection of siGR significantly attenuated MA-induced proliferation, migration, and adipogenic differentiation of ASCs. Although the adipogenic differentiation potential of MA was inferior to that of dexamethasone, MA had mitogenic effects in ASCs. Collectively, these results indicate that MA increases the proliferation, migration, and adipogenic differentiation of ASCs via GR phosphorylation. STEM CELLS TRANSLATIONAL MEDICINE 2015;4:789-799 SIGNIFICANCEMagestrol acetate (MA) increases the proliferation, migration, and adipogenic differentiation of adipose-derived stem cells (ASCs) via glucocorticoid receptor phosphorylation. Therefore, MA can be applied to increase the production yield during expansion and can be used to facilitate adipogenic differentiation of ASCs.

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Estrogen Sulfotransferase/SULT1E1 Promotes Human Adipogenesis

Cited by 49 publications

References 40 publications

Estrogens and Body Weight Regulation in Men

Estrogens and Body Weight Regulation in Men

Estrogen Receptor α and β in Mouse: Adipose-Derived Stem Cell Proliferation, Migration, and Brown Adipogenesis In Vitro

Megestrol Acetate Increases the Proliferation, Migration, and Adipogenic Differentiation of Adipose-Derived Stem Cells via Glucocorticoid Receptor

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