During the mid-cycle LH surge, the granulosa cell shifts from oestrogen production to progesterone production. What molecular mechanism underlies this 'luteinisation' process?

• A LH receptor activation (Gs-cAMP-PKA) upregulates StAR protein for cholesterol transport, shifts steroidogenic enzymes from aromatase-dominant to progesterone-synthetic predominance, and down-regulates LH receptors ✓
• B FSH receptor activation triggers granulosa cell differentiation into luteal cells expressing HCG receptors exclusive to the corpus luteum
• C LH induces oocyte maturation and prostaglandin E2 release, which directly converts granulosa cells to progesterone-secreting luteal cells via COX-2
• D The LH surge activates the Wnt/β-catenin pathway in granulosa cells, suppressing aromatase gene expression via FOXO3

Explanation

The LH surge transforms the pre-ovulatory follicle into the corpus luteum (luteinisation). LH binds its GPCR, activating Gs-adenylyl cyclase-cAMP-PKA. PKA upregulates StAR (steroidogenic acute regulatory protein), which is the rate-limiting step transporting cholesterol from the outer to inner mitochondrial membrane for pregnenolone synthesis. Simultaneously, the pattern of steroidogenic enzymes shifts: expression of CYP17A1 (17α-hydroxylase) falls while 3β-HSD and progesterone synthase predominance rises, redirecting production from oestradiol to progesterone. LH receptor expression is also downregulated (homologous desensitisation). Progesterone from the corpus luteum prepares the endometrium for implantation and is essential for early pregnancy maintenance.

Reference: Guyton & Hall, Textbook of Medical Physiology, 14th ed.

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