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LH promotes testosterone synthesis in rooster leydig cells through YAP1/ACSL4/SOAT1 pathway
Ziming Wang1, Jingxin Pu1, Wen An1
1College of Animal Science and Technology, Jilin Agricultural University, Changchun, 130118, Jilin Province, China; Key Laboratory of the Animal Production, Product Quality and Security, Ministry of Education, Jilin Agricultural University, Changchun, 130118, Jilin Province, China; Jilin Provincial International Joint Research Center of Animal Breeding and Reproduction Technology, Jilin Agricultural University, Changchun, 130118, Jilin Province, China.
Luteinizing hormone (LH) stimulates testosterone production via a new YAP1-ACSL4 pathway. This axis regulates cholesterol metabolism, increasing free cholesterol for steroidogenesis in Leydig cells.
Area of Science:
- Endocrinology
- Molecular Biology
- Lipid Metabolism
Background:
- Testosterone synthesis in Leydig cells is crucial for male reproduction.
- Regulation of testosterone production by luteinizing hormone (LH) and cholesterol metabolism is complex and not fully understood.
Purpose of the Study:
- To elucidate the molecular mechanisms linking LH signaling to testosterone production.
- To identify novel regulators of cholesterol metabolism in Leydig cells involved in steroidogenesis.
Main Methods:
- Transcriptomic profiling of Leydig cells.
- Functional studies involving gene inhibition (YAP1, ACSL4) and expression analysis.
- Analysis of cholesterol esterification and free cholesterol levels.
Main Results:
- A novel YAP1-ACSL4 axis was identified as essential for LH-induced testosterone production.
- LH upregulates YAP1, which increases ACSL4 expression.
- ACSL4, via SOAT1 suppression, enhances free cholesterol availability for testosterone synthesis.
Conclusions:
- The YAP1-ACSL4 axis is a key regulator of cholesterol metabolism and testosterone synthesis in Leydig cells.
- This pathway links gonadotropin signaling to steroidogenesis through modulation of lipid metabolism.
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