scholarly journals Interaction of steroid receptor coactivators and estrogen receptors in the human placenta

2016 ◽  
Vol 56 (3) ◽  
pp. 239-247 ◽  
Author(s):  
Seung Chul Kim ◽  
Mee-Na Park ◽  
Young Joo Lee ◽  
Jong Kil Joo ◽  
Beum-Soo An
Keyword(s):  
Estrogen Receptors ◽  
Human Placenta ◽  
Late Stage ◽  
Clock Gene ◽  
Steroid Receptor ◽  
Estrogen Signaling ◽  
Specific Effects ◽  
Gestation Age ◽  
Steroid Receptor Coactivators ◽  
Estrogen Concentration

Female sex steroid hormones such as estrogen and progesterone have a pivotal role in maintaining pregnancy in human and animals. Especially, estrogen exerts specific effects on the cardiovascular system and angiogenesis, and thus affects significantly on placentation. Although the functions of estrogen have been emphasized during pregnancy, their signaling pathways in the placenta have not been fully understood. In this study, estrogen signaling was evaluated according to gestational age. Human placenta samples were collected and divided into early preterm (n=10), late preterm (n=18), and term (n=20) groups. First, serum estrogen concentration and corticotropin-releasing hormone (CRH) mRNA expression, which is known as gestation clock gene, were increased following gestation age in our experimental condition, as we expected. Next, the expression of estrogen receptors (ERs) and steroid receptor coactivators (SRCs) in the placenta was evaluated. ERα (ESR1) and ERβ (ESR2) were expressed highly at term period compared with early preterm. In addition, SRC family including SRC1, SRC2, and SRC3 was expressed in the human placenta, and the levels of SRC1, SRC2, and SRC3 were increased in the placenta at the late stage of gestation. The interaction of ERs with SRCs was also examined, which was significantly enhanced at term period. In the immunostaining results, it was indicated that ERs and SRCs were all dominantly expressed in syncytiotrophoblast cells. These results suggested that SRC1, SRC2, and SRC3 were expressed and interact with ERs highly at the late stage of gestation, and may amplify the signaling of estrogen in the placenta to maintain pregnancy.

scholarly journals Early and late stage MPN patients show distinct gene expression profiles in CD34+ cells

2021 ◽  
Author(s):  
Julian Baumeister ◽  
Tiago Maié ◽  
Nicolas Chatain ◽  
Lin Gan ◽  
Barbora Weinbergerova ◽  
...  
Keyword(s):  
Gene Expression ◽  
Late Stage ◽  
Rna Splicing ◽  
Bone Marrow Cells ◽  
Myeloproliferative Neoplasms ◽  
Expression Profiles ◽  
Gene Expression Profiles ◽  
Primary Myelofibrosis ◽  
Estrogen Signaling ◽  
Therapeutic Modalities

AbstractMyeloproliferative neoplasms (MPN), comprising essential thrombocythemia (ET), polycythemia vera (PV), and primary myelofibrosis (PMF), are hematological disorders of the myeloid lineage characterized by hyperproliferation of mature blood cells. The prediction of the clinical course and progression remains difficult and new therapeutic modalities are required. We conducted a CD34+ gene expression study to identify signatures and potential biomarkers in the different MPN subtypes with the aim to improve treatment and prevent the transformation from the rather benign chronic state to a more malignant aggressive state. We report here on a systematic gene expression analysis (GEA) of CD34+ peripheral blood or bone marrow cells derived from 30 patients with MPN including all subtypes (ET (n = 6), PV (n = 11), PMF (n = 9), secondary MF (SMF; post-ET-/post-PV-MF; n = 4)) and six healthy donors. GEA revealed a variety of differentially regulated genes in the different MPN subtypes vs. controls, with a higher number in PMF/SMF (200/272 genes) than in ET/PV (132/121). PROGENγ analysis revealed significant induction of TNFα/NF-κB signaling (particularly in SMF) and reduction of estrogen signaling (PMF and SMF). Consistently, inflammatory GO terms were enriched in PMF/SMF, whereas RNA splicing–associated biological processes were downregulated in PMF. Differentially regulated genes that might be utilized as diagnostic/prognostic markers were identified, such as AREG, CYBB, DNTT, TIMD4, VCAM1, and S100 family members (S100A4/8/9/10/12). Additionally, 98 genes (including CLEC1B, CMTM5, CXCL8, DACH1, and RADX) were deregulated solely in SMF and may be used to predict progression from early to late stage MPN. Graphical abstract

scholarly journals Expression of steroid receptor coactivators and corepressors in human endometrial hyperplasia and carcinoma with relevance to steroid receptors and Ki-67 expression

Cancer ◽  
2003 ◽  
Vol 98 (10) ◽  
pp. 2207-2213 ◽  
Author(s):  
Junko Uchikawa ◽  
Tanri Shiozawa ◽  
Hsien-Chang Shih ◽  
Tsutomu Miyamoto ◽  
Yu-Zhen Feng ◽  
...  
Keyword(s):  
Endometrial Hyperplasia ◽  
Steroid Receptors ◽  
Steroid Receptor ◽  
Ki 67 ◽  
Steroid Receptor Coactivators

Expression of Concentrative Nucleoside Transporters (SLC28A) in the Human Placenta: Effects of Gestation Age and Prototype Differentiation-Affecting Agents

2018 ◽  
Vol 15 (7) ◽  
pp. 2732-2741 ◽  
Author(s):  
Lucie Jiraskova ◽  
Lukas Cerveny ◽  
Sara Karbanova ◽  
Zuzana Ptackova ◽  
Frantisek Staud
Keyword(s):  
Human Placenta ◽  
Nucleoside Transporters ◽  
Gestation Age

Membrane-Initiated Estradiol Signaling in the Central Nervous System

2019 ◽  
Author(s):  
Paul E. Micevych ◽  
Melinda A. Mittelman-Smith
Keyword(s):  
Nervous System ◽  
Estrogen Receptor ◽  
Estrogen Receptors ◽  
G Protein ◽  
Nuclear Receptors ◽  
Signaling Cascades ◽  
Estrogen Signaling ◽  
Female Reproduction ◽  
Brain Physiology ◽  
The Brain

In the last two decades of the 20th century, key findings in the field of estrogen signaling completely changed our understanding of hormones: first, steroidogenesis was demonstrated in the CNS; second, a vast majority of cells in the nervous system were shown to have estrogen receptors; third, a second nuclear estrogen receptor (ERß) was cloned; and finally, “nuclear” receptors were shown to be present and functional in the cell membrane. Shortly thereafter, even more membrane estrogen receptors were discovered. Steroids (estrogens, in particular) began to be considered as neurotransmitters and their receptors were tethered to G protein-coupled receptor signaling cascades. In some parts of the brain, levels of steroids appeared to be independent of those found in the circulation and yet, circulating steroids had profound actions on the brain physiology. In this review, we discuss the interaction of peripheral and central estrogen action in the context of female reproduction—one of the best-studied aspects of steroid action. In addition to reviewing the evidence for steroidogenesis in the hypothalamus, we review membrane-localized nuclear receptors coupling to G protein-signaling cascades and the downstream physiological consequences for reproduction. We will also introduce newer work that demonstrates cell signaling for a common splice variant of estrogen receptor-α (ERα), and membrane action of neuroprogesterone in regulating estrogen positive feedback.

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