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Hyperprolactinemia modifies extracellular matrix components associated with collagen fibrillogenesis in harderian glands of non- and pregnant female mice

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Autor(es):
Araujo, Ariadne S. L. ; Simoes, Manuel de J. ; Araujo Jr, Osvaldo P. ; Simoes, Ricardo S. ; Baracat, Edmund C. ; Nader, Helena B. ; Soares Jr, Jose M. ; Gomes, Regina C. T.
Número total de Autores: 8
Tipo de documento: Artigo Científico
Fonte: EXPERIMENTAL EYE RESEARCH; v. 235, p. 10-pg., 2023-10-01.
Resumo

The harderian gland (HG) is a gland located at the base of the nictating membrane and fills the inferomedial aspect of the orbit in rodents. It is under the influence of the hypothalamic-pituitary-gonadal axis and, because of its hormone receptors, it is a target tissue for prolactin (PRL) and sex steroid hormones (estrogen and progesterone). In humans and murine, the anterior surface of the eyes is protected by a tear film synthesized by glands associated with the eye. In order to understand the endocrine changes caused by hyperprolactinemia in the glands responsible for the formation of the tear film, we used an animal model with metoclopramide-induced hyperprolactinemia (HPRL). Given the evidences that HPRL can lead to a process of cell death and tissue fibrosis, the protein expression of small leucine-rich proteoglycans (SLRPs) was analyzed through immunohistochemistry in the HG of the non-and the pregnant female mice with hyperprolactinemia. The SRLPs are related to collagen fibrillogenesis and they participate in pro-apoptotic signals. Our data revealed that high prolactin levels and changes in steroid hormones (estrogen and progesterone) can lead to an alteration in the amount of collagen, and in the structure of type I and III collagen fibers through changes in the amounts of lumican and decorin, which are responsible for collagen fibrillogenesis. This fact can lead to the impaired functioning of the HG by excessive apoptosis in the HG of the non-and the pregnant female mice with HPRL and especially in the HG of pregnancy-associated hyperprolactinemia. (AU)

Processo FAPESP: 11/12417-8 - Expressão gênica dos Pequenos Proteoglicanos Ricos em Leucinas (SLRPS), da prolactina decidual e fatores de crescimentos envolvidos na decidualização do endométrio de camundongos fêmeas com pseudoprenhez com hiperprolactinemia induzida pela metoclopramida
Beneficiário:Regina Célia Teixeira Gomes
Modalidade de apoio: Bolsas no Brasil - Pós-Doutorado