scholarly journals 109 IL-4 and IL-13 cytokines drive sex steroid hormone synthesis and lipid abnormalities in sebocyte during atopic dermatitis pathogenesis

2021 ◽  
Vol 141 (5) ◽  
pp. S20
Author(s):  
C. Zhang ◽  
M. Chinnappan ◽  
M. Artami ◽  
K. Eckert ◽  
G. Vale ◽  
...  
Keyword(s):  
Atopic Dermatitis ◽  
Steroid Hormone ◽  
Sex Steroid ◽  
Sex Steroid Hormone ◽  
Hormone Synthesis ◽  
Lipid Abnormalities

Interleukins 4 and 13 drive lipid abnormalities in skin cells through regulation of sex steroid hormone synthesis

2021 ◽  
Vol 118 (38) ◽  
pp. e2100749118 ◽  
Author(s):  
Chenlu Zhang ◽  
Mahendran Chinnappan ◽  
Courtney A. Prestwood ◽  
Marshall Edwards ◽  
Methinee Artami ◽  
...  
Keyword(s):  
Barrier Function ◽  
Steroid Hormone ◽  
Normal Skin ◽  
Skin Barrier ◽  
Sex Steroid ◽  
Skin Barrier Function ◽  
Sebaceous Glands ◽  
Sex Steroid Hormone ◽  
Hormone Synthesis ◽  
Lipid Abnormalities

Atopic dermatitis (AD) is a chronic inflammatory skin disease characterized by skin dryness, inflammation, and itch. A major hallmark of AD is an elevation of the immune cytokines IL-4 and IL-13. These cytokines lead to skin barrier disruption and lipid abnormalities in AD, yet the underlying mechanisms are unclear. Sebaceous glands are specialized sebum-producing epithelial cells that promote skin barrier function by releasing lipids and antimicrobial proteins to the skin surface. Here, we show that in AD, IL-4 and IL-13 stimulate the expression of 3β-hydroxysteroid dehydrogenase 1 (HSD3B1), a key rate-limiting enzyme in sex steroid hormone synthesis, predominantly expressed by sebaceous glands in human skin. HSD3B1 enhances androgen production in sebocytes, and IL-4 and IL-13 drive lipid abnormalities in human sebocytes and keratinocytes through HSD3B1. Consistent with our findings in cells, HSD3B1 expression is elevated in the skin of AD patients and can be restored by treatment with the IL-4Rα monoclonal antibody, Dupilumab. Androgens are also elevated in a mouse model of AD, though the mechanism in mice remains unclear. Our findings illuminate a connection between type 2 immunity and sex steroid hormone synthesis in the skin and suggest that abnormalities in sex steroid hormone synthesis may underlie the disrupted skin barrier in AD. Furthermore, targeting sex steroid hormone synthesis pathways may be a therapeutic avenue to restoring normal skin barrier function in AD patients.

scholarly journals Response of Sex Steroid Hormone Synthesis Substrates in Serum and Testes of Male Tilapia (Oreochromis niloticus) Exposed to Methomyl and Its Recovery Pattern

2021 ◽  
Vol 11 (22) ◽  
pp. 10997
Author(s):  
Shunlong Meng ◽  
Xi Chen ◽  
Chao Song ◽  
Limin Fan ◽  
Liping Qiu ◽  
...  
Keyword(s):  
Oreochromis Niloticus ◽  
Steroid Hormone ◽  
Free Water ◽  
Sex Steroid ◽  
Toxicity Tests ◽  
Contact Toxicity ◽  
Irreversible Damage ◽  
Sex Steroid Hormone ◽  
Hormone Synthesis ◽  
Reference Threshold

The response of synthetic substrates of sex steroid hormones—cholesterol (CHO), pregnenolone (PREG), and progesterone (PROG)—in the serum and testes of male tilapia (Oreochromis niloticus) to the environmental estrogen pesticide methomyl (0.2, 2, 20, and 200 μg·L−1) was evaluated using static-water contact toxicity tests. The results showed that low methomyl concentrations (0.2 and 2 μg·L−1) had no significant effects on the contents of CHO, PREG, and PROG in the serum and testes of male tilapia (p > 0.05). Consequently, the concentration of 2 μg·L−1 could be used as a preliminary reference threshold for the non-effective dose of methomyl in male tilapia. Exposure to high methomyl concentrations (20 and 200 μg·L−1) significantly inhibited the levels of CHO, PREG, and PROG in the serum and testes of male tilapia (p < 0.05) and showed a dose–response relationship. Sex steroid hormone synthesis substrate damage to male tilapia caused by less than 20 μg·L−1 methomyl was reversible, while the damage caused by equal to or greater than 200 μg·L−1 methomyl was irreversible when tilapia were transferred to methomyl-free water for 18 days. Thus, a concentration of 200 μg·L−1 could be used as a reference threshold for irreversible damage caused by methomyl in male tilapia.

Pelvic floor sex steroid hormone receptors, distribution and expression in pre- and postmenopausal stress urinary incontinent women

2007 ◽  
Vol 86 (11) ◽  
pp. 1377-1384 ◽  
Author(s):  
Marie Westergren Söderberg ◽  
Bengt Johansson ◽  
Britt Masironi ◽  
Birgitta Byström ◽  
Christian Falconer ◽  
...  
Keyword(s):  
Pelvic Floor ◽  
Hormone Receptors ◽  
Steroid Hormone ◽  
Steroid Hormone Receptors ◽  
Sex Steroid ◽  
Sex Steroid Hormone

Immunolocalization of sex steroid hormone receptors in the canine uterine tube and their relation to sex steroid hormone levels

2002 ◽  
Vol 14 (4) ◽  
pp. 241 ◽  
Author(s):  
Hilde Vermeirsch ◽  
Wim Van Den Broeck ◽  
Mark Coryn ◽  
Paul Simoens
Keyword(s):  
Epithelial Cells ◽  
Estrous Cycle ◽  
Stromal Cells ◽  
Hormone Receptors ◽  
Steroid Hormone ◽  
Steroid Hormone Receptors ◽  
Sex Steroid ◽  
Nuclear Staining ◽  
Sex Steroid Hormone ◽  
Uterine Tube

The aim of this immunohistochemical study was to describe the cellular distribution of the estrogen receptor-α (ERα), progesterone receptor (PR) and androgen receptor (AR) in canine uterine tubes. Samples of uterine tubes were taken from dogs in different stages of the estrous cycle, and dogs that were pregnant or had just delivered. Nuclear staining for sex steroid hormone receptors was observed in the surface epithelium, stromal cells and smooth muscle cells of the muscular layer. Only slight differences in staining pattern were observed between the ampulla and fimbriae. The staining for ERα and PR showed changes throughout the estrous cycle. Some of these changes were related to changing concentrations of sex steroid hormones. High staining scores for ERα and PR were found during proestrus and low scores during early metestrus. The staining for AR showed only minor cyclic changes. However, during proestrus and estrus, cytoplasmic staining for AR was observed in differentiated secretory epithelial cells, when nuclear staining in these cells was nearly absent. For the three hormone receptors, stromal cells generally stained with a higher intensity than epithelial cells. It is likely that many steroid hormone actions on the epithelium are mediated through stromal cells. During pregnancy, rather high staining scores were found for ERα and AR in the uterine tube. This is in contrast to observations in the canine pregnant uterus.

scholarly journals Molecular Cloning, Characterization, and Chromosome Mapping of Reptilian Estrogen Receptors

Endocrinology ◽  
2010 ◽  
Vol 151 (12) ◽  
pp. 5710-5720 ◽  
Author(s):  
Yoshinao Katsu ◽  
Kazumi Matsubara ◽  
Satomi Kohno ◽  
Yoichi Matsuda ◽  
Michihisa Toriba ◽  
...  
Keyword(s):  
Estrogen Receptor ◽  
Hormone Receptor ◽  
Molecular Mechanisms ◽  
Steroid Hormone ◽  
Chromosome 1 ◽  
Sex Steroid ◽  
Steroid Hormone Receptor ◽  
Sex Steroid Hormone ◽  
Ligand Interactions ◽  
Rat Snake

In many vertebrates, steroid hormones are essential for ovarian differentiation during a critical developmental stage as well as promoting the growth and differentiation of the adult female reproductive system. Although studies have been extensively conducted in mammals and a few fish, amphibians, and bird species, the molecular mechanisms of sex steroid hormone (estrogens) action have been poorly examined in reptiles. Here, we evaluate hormone receptor and ligand interactions in two species of snake, the Okinawa habu (Protobothrops flavoviridis, Viperidae) and the Japanese four-striped rat snake (Elaphe quadrivirgata, Colubridae) after the isolation of cDNAs encoding estrogen receptor α (ESR1) and estrogen receptor β (ESR2). Using a transient transfection assay with mammalian cells, the transcriptional activity of reptilian (Okinawa habu, Japanese four-striped rat snake, American alligator, and Florida red-belly freshwater turtle) ESR1 and ESR2 was examined. All ESR proteins displayed estrogen-dependent activation of transcription via an estrogen-response element-containing promoter; however, the responsiveness to various estrogens was different. Further, we determined the chromosomal locations of the snake steroid hormone receptor genes. ESR1 and ESR2 genes were localized to the short and long arms of chromosome 1, respectively, whereas androgen receptor was localized to a pair of microchromosomes in the two snake species examined. These data provide basic tools that allow future studies examining receptor-ligand interactions and steroid endocrinology in snakes and also expands our knowledge of sex steroid hormone receptor evolution.

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