Androgen signaling disruption during fetal and postnatal development affects androgen receptor and connexin 43 expression and distribution in adult boar prostate

To date, limited knowledge exists regarding the role of the androgen signaling during specific periods of development in the regulation of androgen receptor (AR) and connexin 43 (Cx43) in adult prostate. Therefore, in this study we examined mRNA and protein expression, and tissue distribution of AR and Cx43 in adult boar prostates following fetal (GD20), neonatal (PD2), and prepubertal (PD90) exposure to an antiandrogen flutamide (50 mg/kg bw). In GD20 and PD2 males we found the reduction of the luminal compartment, inflammatory changes, decreased AR and increased Cx43 expression, and altered localization of both proteins. Moreover, enhanced apoptosis and reduced proliferation were detected in the prostates of these animals. In PD90 males the alterations were less evident, except that Cx43 expression was markedly upregulated. The results presented herein indicate that in boar androgen action during early fetal and neonatal periods plays a key role in the maintenance of normal phenotype and functions of prostatic cells at adulthood. Furthermore, we demonstrated that modulation of Cx43 expression in the prostate could serve as a sensitive marker of hormonal disruption during different developmental stages

Interstitial Leydig cell tumorigenesis : leptin and adiponectin signaling in relation to aromatase expression in the human testis

Although epidemiological studies from the last years report an increase in the incidences of Leydig cell tumors (previously thought to be a rare disease), the biochemical characteristics of that tumor important for understanding its etiology, diagnosis, and therapy still remains not completely characterized. Our prior studies reported G-protein coupled estrogen receptor signaling and estrogen level disturbances in Leydig cell tumors. In addition, we found that expressions of multi-level-acting lipid balance- and steroidogenesis–controlling proteins including peroxisome proliferator-activated receptor are altered in this tumor. In order to get deeper into the other molecular mechanisms that regulate lipid homeostasis in the Leydig cell tumor, here we investigate the presence and expression of newly-described hormones responsible for lipid homeostasis balancing (leptin and adiponectin), together with expression of estrogen synthase (aromatase). Samples of Leydig cell tumors (n = 20) were obtained from patients (31-45 years old) and used for light and transmission electron microscopic, western blotting, and immunohistochemical analyses. In addition, body mass index (BMI) was calculated. In tumor mass, abundant lipid accumulation in Leydig cells and various alterations of Leydig cell shape, as well as the presence of adipocyte-like cells, were observed. Marked lipid content and various lipid droplet size, especially in obese patients, may indicate alterations in lipid homeostasis, lipid processing, and steroidogenic organelle function in response to interstitial tissue pathological changes. We revealed significantly increased expression of leptin, adiponectin and their receptors, as well as aromatase in Leydig cell tumors in comparison to control. The majority of patients (n = 13) were overweight as indicated by their BMI. Moreover, a significant increase in expression of phospholipase C (PLC), and kinases Raf, ERK which are part of adipokine transductional pathways, was demonstrated. These data expand our previous findings suggesting that in human Leydig cell tumors, estrogen level and signaling, together with lipid status, are related to each other. Increased BMI may contribute to certain biochemical characteristics and function of the Leydig cell in infertile patients with a tumor. In addition, altered adipokine-estrogen microenvironment can have an effect on proliferation, growth, and metastasis of tumor cells. We report here various targets (receptors, enzymes, hormones) controlling lipid balance and estrogen action in Leydig cell tumors indicating their possible usefulness for diagnostics and therapy

The role of G-protein-coupled membrane estrogen receptor in mouse Leydig cell function : in vivo and in vitro evaluation

AbstractIn this study, G-coupled estrogen receptor (GPER) was inactivated, by treatment with antagonist (G-15), in testes of C57BL/6 mice: immature (3 weeks old), mature (3 months old) and aged (1.5 years old) (50 μg/kg bw), as well as MA-10 mouse Leydig cells (10 nM/24 h) alone or in combination with 17β-estradiol or antiestrogen (ICI 182,780). In G-15-treated mice, overgrowth of interstitial tissue was found in both mature and aged testes. Depending on age, differences in structure and distribution of various Leydig cell organelles were observed. Concomitantly, modulation of activity of the mitochondria and tubulin microfibers was revealed. Diverse and complex GPER regulation at the mRNA level and protein of estrogen signaling molecules (estrogen receptor α and β; ERα, ERβ and cytochrome P450 aromatase; P450arom) in G-15 Leydig cells was found in relation to age and the experimental system utilized (in vivo and in vitro). Changes in expression patterns of ERs and P450arom, as well as steroid secretion, reflected Leydig cell heterogeneity to estrogen regulation throughout male life including cell physiological status.We show, for the first time, GPER with ERs and P450arom work in tandem to maintain Leydig cell architecture and supervise its steroidogenic function by estrogen during male life. Full set of estrogen signaling molecules, with involvement of GPER, is crucial for proper Leydig cell function where each molecule acts in a specific and/or complementary manner. Further understanding of the mechanisms by which GPER controls Leydig cells with special regard to male age, cell of origin and experimental system used is critical for predicting and preventing testis steroidogenic disorders based on perturbations in estrogen signaling.</jats:p

Ovarian structure and ultrastructure and distribution of endosymbiotic microorganisms in aphid Euceraphis betulae (Hemiptera, Aphidoidea: Aphididae)

W pracy przedstawiono wyniki badań nad strukturą jajnika oraz ultrastrukturą i rozmieszczeniem endosymbiotycznych mikroorganizmów u mszycy Eucerpahis betulae (Hemiptera, Aphidoidea: Aphididae).Jajniki mszyc Euceraphis betulae charakteryzują się budową typową dla wszystkich Hemiptera. Zbudowane są z owariol typu meroistycznego – telotroficznego, w skład których wchodzą cztery elementy: filament terminalny, trofarium, witelarium i nóżka owarialna, zwana pedicelem.Jajniki samic pokolenia jajorodnego składają się z sześciu owariol, a żyworodnych z pięciu. Trofaria są otoczone osłonką wewnątrzowarialną. Komory odżywcze obu pokoleń zawierają w części apikalnej i środkowej komórki odżywcze, nazywane trofocytami, a w części bazalnej oocyty prewitelogeniczne, czyli oocyty zatrzymane w rozwoju. Samice jajorodne posiadają 36 – 43 komórek płciowych w owarioli, natomiast żyworodne 28 – 33. W części centralnej komory odżywczej, znajduje się rdzeń odżywczy. Rdzeń odżywczy silniej rozgałęzia się u samic jajorodnych. Z rdzeniem, za pomocą wypustek cytoplazmatycznych, połączone są trofocyty. Sznur odżywczy łączy rdzeń odżywczy z oocytem w witelarium. W witelarium samic jajorodnych rozwija się 1 lub 2 oocyty, a żyworodnych tylko 1. U obu pokoleń oocyt w witelarium otoczony jest jednowarstwowym nabłonkiem folikularnym.Bakteria Buchnera aphidicola przekazywana jest do następnego pokolenia na drodze transportu transowarialnego. Infekuje ona oocyty oraz zarodki.This paper presents results of studies of the ovary structure, and ultrastructure and distribution of endosymbiotic microorganisms in Eucerpahis betulae aphid (Hemiptera, Aphidoidea: Aphididae).Ovaries of Euceraphis betulae aphids are typical of the Hemiptera structure. They are constructed of meroistic – telotrophic ovarioles comprised of four elements: terminal filament, tropharium, vitellarium and pedicel.The ovaries of oviparous generation consist of six ovarioles when viviparous have five ovarioles per ovary. Trophic chambers of both generations contain trophocytes in the apical and middle area, and in basal area there are previtellogenic oocytes called arrested oocytes. Oviparous females have 36 - 43 germ cells in ovarioles and the viviparous females have 28 - 33. In the central region of the trophic chamber there is a trophic core. The trophic core is more branched in oviparous females. Trophocytes are connected with trophic core by cytoplasmic tabs. Nutritive cord is connecting trophic core with oocyte in vitellarium. Vitellarium of oviparous females develops 1 or 2 oocytes, and viviparous generation have 1 oocyte. In both generations oocytes in vitellarium is surrounded by one-layer follicular epithelium. Euceraphis betulae has only one type of endosymbiotic microorganism - Buchnera aphidicola bacterium. This bacterium is transovarially transmitted from mother to the next generations. Buchnera aphidicola infects the oocytes and embryos