ArticleEndocrinology2013
Precocious puberty and Leydig cell hyperplasia in male mice with a gain of function mutation in the LH receptor gene.
Article in Endocrinology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 57 citations in OpenAlex.
- TransgenicPharmaceuticals (Basel, Switzerland) · 2024Article
- Elevated luteinizing hormone receptor signaling or selenium treatment leads to comparable changes in adrenal cortex histology and androgen-AR/ZIP9 signaling.Protoplasma · 2024Article
- Familial male-limited precocious puberty due to an activating mutation of the LHCGR: a case report and literature review.Annals of pediatric endocrinology & metabolism · 2024Article
- Specific Signal Transduction of Constitutively Activating (D576G) and Inactivating (R476H) Mutants of Agonist-Stimulated Luteinizing Hormone Receptor in Eel.International journal of molecular sciences · 2023Article
- Revisiting the gonadotropic regulation of mammalian spermatogenesis: evolving lessons during the past decade.Frontiers in endocrinology · 2023Review
- Single-Step Protocol for Isolating the Recombinant Extracellular Domain of the Luteinizing Hormone Receptor from theCurrent issues in molecular biology · 2022Article
- Leydig Cell-Specific DAX1-Deleted Mice Has Higher Testosterone Level in the Testis During Pubertal Development.Reproductive sciences (Thousand Oaks, Calif.) · 2022Article
- Long-Term Treatment With Letrozole in a Boy With Familial Male-Limited Precocious Puberty.Frontiers in endocrinology · 2022Article
- Cell-Surface Loss of Constitutive Activating and Inactivating Mutants of Eel Luteinizing Hormone Receptors.Development & reproduction · 2021Article
- Protein kinase A drives paracrine crisis and WNT4-dependent testis tumor in Carney complex.The Journal of clinical investigation · 2021Article
- Constitutive Activating Eel Luteinizing Hormone Receptors Induce Constitutively Signal Transduction and Inactivating Mutants Impair Biological Activity.Development & reproduction · 2021Article
- Constitutive LH receptor activity impairs NO-mediated penile smooth muscle relaxation.Reproduction (Cambridge, England) · 2021Article
- Neuropilin-1 expression in GnRH neurons regulates prepubertal weight gain and sexual attraction.The EMBO journal · 2020Article
- Immunohistochemical localization and possible functions of nesfatin-1 in the testis of mice during pubertal development and sexual maturation.Journal of molecular histology · 2019Article
- Altered hormonal milieu and dysregulated protein expression can cause spermatogenic arrest in ectopic xenografted immature rat testis.Scientific reports · 2019Article
- Comparing Postnatal Development of Gonadal Hormones and Associated Social Behaviors in Rats, Mice, and Humans.Endocrinology · 2018Review
- Suppression of luteinizing hormone enhances HSC recovery after hematopoietic injury.Nature medicine · 2018Article
- Minireview: Insights Into the Structural and Molecular Consequences of the TSH-β Mutation C105Vfs114X.Molecular endocrinology (Baltimore, Md.) · 2016Review
- Hyperplasia in glands with hormone excess.Endocrine-related cancer · 2016Review
- Expressions of Sox9, Sox5, and Sox13 transcription factors in mice testis during postnatal development.Molecular and cellular biochemistry · 2015Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
The LH receptor (LHR) is critical for steroidogenesis and gametogenesis. Its essential role is underscored by the developmental and reproductive abnormalities that occur due to genetic mutations identified in the human LHR. In males, activating mutations are associated with precocious puberty and Leydig cell hyperplasia. To generate a mouse model for the human disease, we have introduced an aspartic acid to glycine mutation in amino acid residue 582 (D582G) of the mouse LHR gene corresponding to the most common D578G mutation found in boys with familial male-limited precocious puberty (FMPP). In transfected cells, mouse D582G mLHR exhibited constitutive activity with a 23-fold increase in basal cAMP levels compared with the wild-type receptor. A temporal study of male mice from 7 days to 24 weeks indicated that the knock-in mice with the mutated receptor (KiLHR(D582G)) exhibited precocious puberty with elevated testosterone levels as early as 7 days of age and through adulthood. Leydig cell-specific genes encoding LHR and several steroidogenic enzymes were up-regulated in KiLHR(D582G) testis. Leydig cell hyperplasia was detected at all ages, whereas Sertoli and germ cell development appeared normal. A novel finding from our studies, not previously reported in the FMPP cases, is that extensive hyperplasia is commonly found around the periphery of the testis. We further demonstrate that the hyperplasia is due to premature proliferation and precocious differentiation of adult Leydig cells in the KiLHR(D582G) testis. The KiLHR(D582G) mice provide a mouse model for FMPP, and we suggest that it is a useful model for studying pathologies associated with altered LHR signaling.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.