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Genetic Models for the Study of Luteinizing Hormone Receptor Function.
1Department of Physiology, School of Medicine, Southern Illinois University , Carbondale, IL , USA.
Frontiers in Endocrinology
|October 21, 2015
Summary
The luteinizing hormone/chorionic gonadotropin receptor (LHCGR) is vital for fertility and sexual development. Genetically modified mouse models reveal how LHCGR function impacts reproductive health and disorders.
Area of Science:
- Reproductive Biology
- Endocrinology
- Molecular Genetics
Background:
- The luteinizing hormone/chorionic gonadotropin receptor (LHCGR) is crucial for human fertility, mediating signaling for steroidogenesis, gametogenesis, and male sexual differentiation.
- Naturally occurring mutations in LHCGR lead to various reproductive disorders, highlighting its critical role.
Purpose of the Study:
- To review findings from genetically modified mouse models investigating LHCGR function.
- To elucidate the physiological and pathological consequences of altered LHCGR signaling.
Main Methods:
- Analysis of mouse models with targeted deletion of LH and LHCGR, mimicking inactivating mutations.
- Study of mice expressing constitutively active LHCGR mutants, mimicking activating mutations.
- Examination of transgenic models with LH and hCG overexpression.
Main Results:
- These models effectively recapitulate reproductive disorders caused by LHCGR dysfunction.
- Loss-of-function models demonstrate LHCGR's necessity in reproductive processes.
- Gain-of-function models illustrate the effects of constitutive LHCGR activation.
Conclusions:
- Genetically modified mouse models are invaluable tools for studying LHCGR signaling in reproductive physiology and pathology.
- Understanding LHCGR function through these models advances knowledge of fertility and related disorders.
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