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Hormonal Regulation in the Treatment of Fibroids
Published in John C. Petrozza, Uterine Fibroids, 2020
Victoria Fitz, Steven L. Young
Leiomyomata (fibroids) are common, monoclonal, proliferative and fibrotic lesions of the uterine smooth muscle. Although fibroid pathogenesis remains unclear, genetics and micronutrients appear to play a role. Additionally, fibroids are highly dependent on sex steroids for growth and maintenance. The aim of this chapter is to review current knowledge regarding the pathophysiological mechanisms of sex steroid action and the current and future role of sex steroid-receptor modulating agents (SSMAs) for therapeutic benefit.
Hormones as Immune Modulating Agents
Published in Thomas F. Kresina, Immune Modulating Agents, 2020
Estrogen and androgen receptors are present in the thymus and in the bursa of Fabricius; however, classical estrogen receptors (detectable by the dextran-coated charcoal assay) in secondary lymphoid tissue are not present, with the exception of CD8+ T lymphocytes, which express receptors for estradiol. Progesterone is capable of acting through GC receptors, although the existence of specific receptors for this hormone in lymphoid cells has also been described. At high concentrations estrogens and androgens also act on GC receptors [26,240–242]. There are indications for the existence of as yet unidentified steroid receptors that affect lymphocyte reactions. For instance, estradiol and triphenylethylene antiestrogens (e.g., tamoxifen or toremifene) both sensitize lymphoid and nonlymphoid target cells for cell-mediated killing in the absence of classical estrogen receptors. This finding suggests the existence of a novel steroid receptor on which both estradiol and antiestrogens act synergistically rather than antagonistically [243]. Membrane-bound steroid receptors which include the polyglycoprotein (PGP) pump have also been described. Triphenylethylene-derived antiestrogens are capable of inhibiting lymphocyte proliferation under conditions in which estradiol has no effect. A membrane-bound antiestrogen binding site for which the natural ligand is unknown seems to be involved in this phenomenon [243].
Steroid Receptors in the Pregnant Uterus*
Published in Gabor Huszar, The Physiology and Biochemistry of the Uterus in Pregnancy and Labor, 2020
Hideki Sakamoto, Neil MacLusky, Frederick Naftolin
The native cytoplasmic and nuclear forms of different steroid receptors share a number of common physicochemical properties. They are all proteins that bind their respective hormonal steroids specificially and with high affinity (equilibrium dissociation constant, or “Kd”, in the range 10-11 to 10-8M). This property enables them to be studied experimentally and assayed relatively easily, since the tightly bound complexes formed between radiolabeled steroids and the receptors can be separated from unbound and lower-affinity-bound steroids by a variety of rapid separation techniques (for review see Clark and Peck6).
Anterior Migration of Triamcinolone Acetonide after Posterior Subtenon Injection for Macular Edema Predisposes to Intraocular Pressure Elevation
Published in Current Eye Research, 2021
Yun-Hsiang Yang, Wei-Cherng Hsu, Yi-Ting Hsieh
Posterior subtenon injection of triamcinolone acetonide (PSTA) is an effective low-cost, off-label treatment for macular edema due to various diseases, such as diabetic macular edema (DME), retinal vein occlusion (RVO), pseudophakic cystoid macular edema (CMO), or uveitis.1–4 However, one of the most important side effects of PSTA is ocular hypertension or secondary glaucoma.5–10 It is proposed that steroid-induced intraocular pressure (IOP) elevation results from the increased resistance to aqueous outflow via the trabecular meshwork (TM).11 Steroids activate the steroid receptors on trabecular cells and alter their gene expression, thereby increasing glycoprotein synthesis and accumulation within the extracellular matrix. Changes in the microstructure of the TM and its cellular activity lead to a progressive accumulation of cell debris and increased resistance to the aqueous outflow.12
Pyroptosis and inflammasomes in obstetrical and gynecological diseases
Published in Gynecological Endocrinology, 2021
The steroid receptor coactivator-1 isoform/estrogen receptor-β axis has a crutial role in endometriosis progression. Dr. Cho Y’s research team finds that serving as inhibitor of steroid receptor coactivator, Bufalin is able to effectively increase steroid receptor coactivator-1 isoform protein stability as well as hyperactivate the steroid receptor coactivator-1 isoform transcriptional activity in endometriotic lesions. Therefore, the drug disrupts the functional axis of steroid receptor coactivator-1 isoform/estrogen receptor-β. In the stromal cells of endometriotic lesions from mice models with surgically induced endometriosis, Bufalin treatment increases the levels of caspase-1 and the active form of IL-1β. It induced pyroptosis and apoptosis in endometriotic lesions, thus, reduced proliferation and eventually suppressed the growth of endometriotic lesions significantly [39]. In this case, future generations of steroid receptor coactivator-modulators could be employed as an alternative medical approach for endometriosis treatment.
Glucocorticoid-induced ocular hypertension: origins and new approaches to minimize
Published in Expert Review of Ophthalmology, 2020
Thomas Yorio, Gaurang C. Patel, Abbot F. Clark
GC-induced gene expression is cell-type and tissue-type dependent, which is dependent on chromatin accessibility and GR-binding site availability. Furthermore, co-activators that influence posttranslational modifications of histones (acetylation and methylation), act as integrators of transcriptional regulation of GRα [4,34]. The steroid receptor co-activator (SRC) family of proteins contribute to GR transactivation. These co-activators alter chromatin structure making it more accessible to general TFs and the RNA polymerase complex, further stabilizing the transcriptional machinery leading to enhanced transcription of steroid-activated genes. Some of the effects of GCs on the TM are likely due to varying expressions of these co-activators. In a recent study, Bermudez et al. [35] used RNA sequencing to identify 93 and 606 differentially expressed genes in different expression groups between GC responder and non-responder in bovine TM cells encompassing 35 pathways associated with these differentially expressed genes using RNA sequencing. Since human and bovine have similar GC responder rate [36], these genes and pathways might explain differential GC responsiveness in the human eye. However, we still need to know the exact function of each gene/pathway in GC-induced OHT and GC-induced glaucoma and its potential correlation to human studies.