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      Sexual Dimorphism in the Regulation of Estrogen, Progesterone, and Androgen Receptors by Sex Steroids in the Rat Airway Smooth Muscle Cells

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          Abstract

          The role of sex hormones in lung is known. The three main sex steroid receptors, estrogen, progesterone, and androgen, have not been sufficiently studied in airway smooth muscle cells (ASMC), and the sex hormone regulation on these receptors is unknown. We examined the presence and regulation of sex hormone receptors in female and male rat ASMC by Western blotting and flow cytometry. Gonadectomized rats were treated with 17 β-estradiol, progesterone, 17 β-estradiol + progesterone, or testosterone. ASMC were enzymatically isolated from tracheas and bronchi. The experiments were performed with double staining flow cytometry (anti- α-actin smooth muscle and antibodies to each hormone receptor). ER α, ER β, tPR, and AR were detected in females or males. ER α was upregulated by E2 and T and downregulated by P4 in females; in males, ER α was downregulated by P4, E + P, and T. ER β was downregulated by each treatment in females, and only by E + P and T in males. tPR was downregulated by P4, E + P, and T in females. No hormonal regulation was observed in male receptors. AR was downregulated in males treated with E + P and T. We have shown the occurrence of sex hormone receptors in ASMC and their regulation by the sex hormones in female and male rats.

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          Most cited references34

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          Mortality from pulmonary fibrosis increased in the United States from 1992 to 2003.

          From the late 1970s to the early 1990s, studies found that mortality rates for pulmonary fibrosis were increasing. Recent data for mortality from pulmonary fibrosis are unavailable. We sought to determine mortality rates for pulmonary fibrosis in the United States from 1992 through 2003. Using data from the National Center for Health Statistics, we calculated age-adjusted mortality rates from the deaths of persons with pulmonary fibrosis and stratified the data to determine differences in mortality rates by age, sex, race/ethnicity, and geography of the decedent. We developed a multivariable model to predict future mortality rates, and we determined the underlying cause of death in patients with pulmonary fibrosis. From 1992 to 2003, there were 28,176,224 deaths in the United States and 175,088 decedents with pulmonary fibrosis. The average age- and sex-adjusted mortality rate was 50.8 per 1,000,000 people. The age-adjusted mortality rate increased 28.4% in men (from 40.2 deaths per 1,000,000 in 1992 to 61.9 deaths per 1,000,000 in 2003) and 41.3% in women (from 39.0 deaths per 1,000,000 in 1992 to 55.1 deaths per 1,000,000 in 2003). While increases were significant in both men and women (p < 0.0001), the rate of increase was higher in women (p < 0.0001). The most common cause of death in patients with pulmonary fibrosis was the disease itself. From 1992 to 2003, mortality rates for pulmonary fibrosis significantly increased. Further investigation is needed to determine the etiology of these trends, which are predicted to continue to increase.
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            It's all about sex: gender, lung development and lung disease.

            Accumulating evidence suggests that gender affects the incidence, susceptibility and severity of several lung diseases. Gender also influences lung development and physiology. Data from both human and animal studies indicate that sex hormones might contribute to disease pathogenesis or serve as protective factors, depending on the disease involved. In this review, the influence of gender and sex hormones on lung development and pathology will be discussed, with specific emphasis on pulmonary fibrosis, asthma and cancer.
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              Phosphorylation of human progesterone receptors at serine-294 by mitogen-activated protein kinase signals their degradation by the 26S proteasome.

              Ligand-dependent down-regulation that leads to rapid and extensive loss of protein is characteristic of several nuclear steroid receptors, including human progesterone receptors (PRs). In breast cancer cells, >95% of PRs are degraded 6 h after the start of progestin treatment. The mechanism for down-regulation is unknown. We examined the role of PR phosphorylation by mitogen-activated protein kinases (MAPKs) in this process. Lactacystin and calpain inhibitor I, specific inhibitors of the 26S proteasome, blocked progestin-induced down-regulation, and ubiquitinated conjugates of PR accumulated in cells. Ligand-dependent PR degradation was also blocked by specific inhibition of p42 and p44 MAPKs. To define the targets of phosphorylation by this kinase, two serine/proline MAPK consensus sites on PR were mutated. We demonstrate that mutation of PR serine-294 to alanine (S294A) specifically and completely prevents ligand-dependent receptor down-regulation. We also find that rapid, ligand-independent degradation of immature PR intermediates occurs by a proteasome-mediated pathway. These results demonstrate that PR destruction, by either of two alternate routes, is mediated by the 26S proteasome. Specifically, down-regulation of mature PRs occurs by a mechanism in which ligand binding activates PR phosphorylation by MAPKs at a unique serine residue, which then targets the receptors for degradation.
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                Author and article information

                Journal
                Int J Endocrinol
                Int J Endocrinol
                IJE
                International Journal of Endocrinology
                Hindawi Publishing Corporation
                1687-8337
                1687-8345
                2016
                24 March 2016
                : 2016
                : 8423192
                Affiliations
                1Unidad de Investigación Médica en Farmacología, Hospital de Especialidades, Centro Médico Nacional Siglo XXI, 06725 Ciudad de México, Mexico
                2Departamento de Medicina Genómica y Toxicología Ambiental, Instituto de Investigaciones Biomédicas, Universidad Nacional Autónoma de México, Ciudad Universitaria, 04510 Ciudad de México, Mexico
                3Facultad de Ciencias Químicas de la Universidad La Salle, 06140 Ciudad de México, Mexico
                4Departamento de Hiperreactividad Bronquial, Instituto Nacional de Enfermedades Respiratorias Ismael Cosío Villegas, 14080 Ciudad de México, Mexico
                5Hospital Infantil de México Federico Gómez, 06720 Ciudad de México, Mexico
                Author notes
                *María G. Campos-Lara: mariagcampos@ 123456yahoo.com

                Academic Editor: Małgorzata Kotula-Balak

                Article
                10.1155/2016/8423192
                4823480
                27110242
                694cbddb-e481-4119-b274-e33bfcbfc7c3
                Copyright © 2016 Abraham Zarazúa et al.

                This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                : 16 October 2015
                : 24 February 2016
                : 24 February 2016
                Categories
                Research Article

                Endocrinology & Diabetes
                Endocrinology & Diabetes

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