Mouse Anti-Human Estrogen Receptor monoclonal antibody, clone JID514

Environmental estrogens from anthropogenic activities are ubiquitous in aquatic ecosystems. Ambient temperature in these systems also fluctuates in daily, seasonal, and long-term rhythms. While both factors have been studied extensively, their interaction on aquatic life is critical to understand. The objective of this study was, therefore, to examine how behavior and gene expression are impacted by estrogenic exposure across a range of environmental temperatures. Larval fathead minnows (Pimephales promelas) were exposed to estrone (E-1) at two concentrations (nominal 625 and 1250 ng/L) or to an ethanol solvent control, at one of four temperatures (15, 18, 21 and 24 degrees C) from fertilization to 21 days post-hatch. Exposed larvae were assessed for alterations in predator evasion performance and mRNA abundances of two genes for calcium channel receptors found in muscles - dihydropyridine receptor (dhpr) and ryanodine receptor 1, and the gonadal genes anti-Mullerian hormone, cytochrome P450 gonadal aromatase (cyp19a), doublesex and mab-3 related transcription factor 1 (dmrt1) and estrogen receptor 1 (esr1). Larval escape angle, escape latency, as well as systemic esr1 and cyp 19a mRNA abundances were altered by an interaction between E-1 concentration and temperature. E-1-exposed larval exhibited reduced escape performance across all tested temperatures, whereas decreased systemic dhpr mRNA abundance was observed only at 18 degrees C. E-1-exposure reduced systemic mRNA abundances of amh, cyp19a, dhpr, and ryr1, while temperature significantly reduced systemic cyp19a and dhpr mRNA abundances. E-1-exposure and temperature significant enhanced systemic mRNA abundances of esr1 and cyp19a, respectively. These complex results illustrate the importance of considering how abiotic factors may moderate the effects of contaminant exposure during the sensitive larval developmental stage, as temperature modulates effects of estrogenic exposure on animal performance and mRNA abundances. (C) 2019 Elsevier B.V. All rights reserved.

The mechanism of gender disparity in cutaneous melanoma incidence remains unclear. Steroid hormones including estrogens have long been implicated in the course of melanoma, but the conclusion is controversial. Estrogen receptors (ERs) and insulin-like growth factor 1 receptor (IGF1R) show extensive crosstalk in cancer development, but how the ER/IGF1R network impacts melanoma is currently unclear. Here we studied the melanoma associations of selected SNPs from the ER/IGF1R network. Part of the International Genes, Environment, and Melanoma (GEM) cohort was used as a discovery set, and the Gene Environment Association Studies Initiative (GENEVA) dataset served as a validation set. Based on the associations with other malignant disease conditions, thirteen single nucleotide polymorphism (SNP) variants in ESR1, ESR2, IGF1, and IGF1R were selected for candidate gene association analyses. The rs1520220 in IGF1 and rs2229765 in IGF1R variants were significantly associated with melanoma risk in the GEM dataset after Benjamini-Hochberg multiple comparison correction, although they were not validated in the GENEVA set. The discrepancy may be caused by the multiple melanoma characteristics in the GEM patients. Further analysis of gender disparity was carried out for IGF1 and IGF1R SNPs in the GEM dataset. The GG phenotype in IGF1 rs1520220 (recessive model) presented an increased risk of melanoma (OR = 8.11, 95% CI: 2.20, 52.5, p = 0.006) in men but a significant opposite effect in women (OR = 0.15, 95% CI: 0.018, 0.86, p = 0.045). The AA genotype in IGF1R rs2229765 (recessive model) showed a significant protective effect in men (OR = 0.24, 95% CI: 0.07, 0.64, p = 0.008) and no effect in women. Results from the current study are warranted for further validation.