Hypothyroidism induces uterine hyperplasia and inflammation related to sex hormone receptors expression in virgin rabbits
Por:
Rodriguez-Castelan, Julia, Del Moral-Morales, Aylin, Gabriela Pina-Medina, Ana, Zepeda-Perez, Dafne, Castillo-Romano, Marlenne, Mendez-Tepepa, Maribel, Espindola-Lozano, Marlen, Camacho-Arroyo, Ignacio, Cuevas-Romero, Estela
Publicada:
1 ago 2019
Resumen:
Aims: In women, uterine alterations have been associated with sex
steroid hormones. Sex hormones regulate the expression of thyroid
hormone receptors (TRs) in the uterus, but an inverse link is unknown.
We analyzed the impact of hypothyroidism on histological
characteristics, vascular endothelial growth factor (VEGF-A),
progesterone receptors (PR), estrogen receptors (ER), thyroid hormone
receptors (TRs), perilipin (PLIN-A), and lipid content in the uterus of
virgin rabbits.
Main methods: Twelve Chinchilla-breed adult female rabbits were grouped
into control (n = 6) and hypothyroid (n = 6; 0.02% of methimazole for
30 days). The thickness of endometrium and myometrium, number of uterine
glands, and infiltration of immune cells were analyzed. The expression
of VEGF-A, PR, ERa, and PLIN-A was determined by RT-PCR and western
blot. The uterine content of triglycerides (TAG), total cholesterol
(TC), and malondialdehyde (MDA) was quantified.
Key findings: Hypothyroidism promoted uterine hyperplasia and a high
infiltration of immune cells into the endometrium, including macrophages
CD163 + It also increased the expression of VEGF-A, TRA, and ER alpha-66
but reduced that of PR and ER alpha-46. The uterine content of PLIN-A,
TAG, and TC was reduced, but that of MDA was augmented in hypothyroid
rabbits.
Significance: Our results suggest that uterine hyperplasia and
inflammation promoted by hypothyroidism should be related to changes in
the VEGF-A, PR, ER, and TRs expression, as well as to modifications in
the PLIN-A expression, lipid content, and oxidative status. These
results suggest that hypothyroidism should affect the fertility of
females.
Filiaciones:
Rodriguez-Castelan, Julia:
Univ Autonoma Tlaxcala, Ciencias Biol, Tlaxcala, Mexico
Univ Nacl Autonoma, Inst Neurobiol, Dept Neurobiol Celular & Mol, Mexico City, DF, Mexico
Doctorado en Ciencias Biológicas, Universidad Autónoma de Tlaxcala, Tlaxcala, Mexico
Departamento de Neurobiología Celular y Molecular, Instituto de Neurobiología, Universidad Nacional Autónoma de, Mexico
Del Moral-Morales, Aylin:
Univ Nacl Autonoma Mexico, Fac Quim, Inst Nacl Perinatol, Unidad Invest Reprod Humana, Ciudad De Mexico, Mexico
Unidad de Investigación en Reproducción Humana, Instituto Nacional de Perinatología-Facultad de Química, Universidad Nacional Autónoma de México, Ciudad de México, Mexico
Gabriela Pina-Medina, Ana:
Univ Nacl Autonoma Mexico, Dept Biol, Fac Quim, Ciudad De Mexico, Mexico
Zepeda-Perez, Dafne:
Univ Autonoma Tlaxcala, Ciencias Biol, Tlaxcala, Mexico
Maestría en Ciencias Biológicas, Universidad Autónoma de Tlaxcala, Tlaxcala, Mexico
Castillo-Romano, Marlenne:
Univ Autonoma Tlaxcala, Ciencias Biol, Tlaxcala, Mexico
Maestría en Ciencias Biológicas, Universidad Autónoma de Tlaxcala, Tlaxcala, Mexico
Mendez-Tepepa, Maribel:
Univ Autonoma Tlaxcala, Ciencias Biol, Tlaxcala, Mexico
Doctorado en Ciencias Biológicas, Universidad Autónoma de Tlaxcala, Tlaxcala, Mexico
Espindola-Lozano, Marlen:
Univ Autonoma Tlaxcala, Ciencias Biol, Tlaxcala, Mexico
Doctorado en Ciencias Biológicas, Universidad Autónoma de Tlaxcala, Tlaxcala, Mexico
Camacho-Arroyo, Ignacio:
Univ Nacl Autonoma Mexico, Fac Quim, Inst Nacl Perinatol, Unidad Invest Reprod Humana, Ciudad De Mexico, Mexico
Unidad de Investigación en Reproducción Humana, Instituto Nacional de Perinatología-Facultad de Química, Universidad Nacional Autónoma de México, Ciudad de México, Mexico
Cuevas-Romero, Estela:
Univ Autonoma Tlaxcala, Ctr Tlaxcala Biol Conducta, Carretera Tlaxcala Puebla Km 1-5, Tlaxcala 90062, Mexico
Centro Tlaxcala de Biología de la Conducta, Universidad Autónoma de Tlaxcala, Tlaxcala, Mexico
Facultad de Química, Departamento de Biología, Universidad Nacional Autónoma de México, Ciudad de México, Mexico
|