Persistently expressed human chorionic gonadotropin induces premature luteinization and progressive alterations on the reproductive axis in female mice

•Elevated human chorionic gonadotropin hormone (hCG) induced female infertility.•A progressive impairment of the reproductive function occurred from peripuberty.•Persistently elevated levels of hCG induced prolactin synthesis and secretion.•Elevated hCG and prolactin induced premature luteinization...

Celý popis

Uložené v:
Podrobná bibliografia
Vydané v:General and comparative endocrinology Ročník 336; s. 114247
Hlavní autori: Marcial Lopez, Agustina, Ratner, Laura D., Martinez, Carolina S., Di Giorgio, Noelia, Poutanen, Matti, Huhtaniemi, Ilpo T., Rulli, Susana B.
Médium: Journal Article
Jazyk:English
Vydavateľské údaje: United States Elsevier Inc 15.05.2023
Predmet:
Animals
beta Subunit
Chorionic Gonadotropin
Chorionic Gonadotropin - pharmacology
Chorionic Gonadotropin, beta Subunit, Human - genetics
Chorionic Gonadotropin, beta Subunit, Human - metabolism
Endocrinology and Diabetes
Endokrinologi och diabetes
Female
Female reproduction
genetics
Human
Human chorionic gonadotropin
Humans
Infertility
Luteinization
Mammals
Mammals - metabolism
metabolism
Mice
Mice, Transgenic
Ovary
pharmacology
Premature luteinization
Prolactin
Transgenic
Transgenic mice
Premature luteinization
Ovary
Female reproduction
Prolactin
Human chorionic gonadotropin
Transgenic mice
ISSN:0016-6480, 1095-6840, 1095-6840
On-line prístup:Získať plný text
Tagy: Pridať tag
Žiadne tagy, Buďte prvý, kto otaguje tento záznam!
Popis
Shrnutí:•Elevated human chorionic gonadotropin hormone (hCG) induced female infertility.•A progressive impairment of the reproductive function occurred from peripuberty.•Persistently elevated levels of hCG induced prolactin synthesis and secretion.•Elevated hCG and prolactin induced premature luteinization of the ovary and progesterone synthesis.•Transgenic female mice overexpressing hCG became a suitable model to study hyperprolactinemia. The hypothalamic–pituitary–gonadal axis plays a fundamental role in the endocrine regulation of the reproductive function in mammals. Any change in the function of the participating hormones or their receptors can lead to alterations in sexual differentiation, the onset of puberty, infertility, cancer development, and other dysfunctions. In this study, we analyzed the influence of persistently elevated levels of the human chorionic gonadotropin hormone (hCG), a powerful agonist of pituitary luteinizing hormone (LH), on the reproductive axis of female mice. As a consequence of chronic hCG hypersecretion through a global expression of the hCGbeta-subunit in transgenic (TG) female mice, a series of events perturbed the prepubertal to juvenile transition. The imbalance in gonadotropin action was first manifested by precocious puberty and alterations in gonadal hormone production, with the consequent ovarian function disruption and infertility in adulthood. The expansion of cumulus cells in vivo and in vitro, ovulatory capacity, and gene expression of ovulation-related marker genes after hormone stimulation were normal in 3-week-old TG females. However, the expression of genes related to steroidogenesis and luteinization such as Lhcgr, Prlr, and the steroidogenic enzymes Cyp11a1, Cyp17a1, and Cyp19a1 were significantly elevated in the TG females. This study demonstrates that the excessive secretion of hCG in concert with high prolactin, induced premature luteinization, and enhanced ovarian steroidogenesis, as was shown by the up-regulation of luteal cell markers and progesterone synthesis in the TG mice. Furthermore, progressively impaired reproductive function of the TG females occurred from the peripubertal stage to adulthood, thus culminating in infertility.
Bibliografia:ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
content type line 23
ISSN:0016-6480
1095-6840
1095-6840
DOI:10.1016/j.ygcen.2023.114247