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Int J Endocrinol. 2016;2016:8423192. doi: 10.1155/2016/8423192. Epub 2016 Mar 24.

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

International journal of endocrinology

Abraham Zarazúa, Aliesha González-Arenas, Gabriela Ramírez-Vélez, Blanca Bazán-Perkins, Christian Guerra-Araiza, María G Campos-Lara

Affiliations

  1. Unidad de Investigación Médica en Farmacología, Hospital de Especialidades, Centro Médico Nacional Siglo XXI, 06725 Ciudad de México, Mexico.
  2. Departamento de Medicina Genómica y Toxicología Ambiental, Instituto de Investigaciones Biomédicas, Universidad Nacional Autónoma de México, Ciudad Universitaria, 04510 Ciudad de México, Mexico.
  3. Facultad de Ciencias Químicas de la Universidad La Salle, 06140 Ciudad de México, Mexico.
  4. Departamento de Hiperreactividad Bronquial, Instituto Nacional de Enfermedades Respiratorias Ismael Cosío Villegas, 14080 Ciudad de México, Mexico.
  5. Unidad de Investigación Médica en Farmacología, Hospital de Especialidades, Centro Médico Nacional Siglo XXI, 06725 Ciudad de México, Mexico; Hospital Infantil de México Federico Gómez, 06720 Ciudad de México, Mexico.

PMID: 27110242 PMCID: PMC4823480 DOI: 10.1155/2016/8423192

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 17β-estradiol, progesterone, 17β-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). ERα, ERβ, tPR, and AR were detected in females or males. ERα was upregulated by E2 and T and downregulated by P4 in females; in males, ERα was downregulated by P4, E + P, and T. ERβ 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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