What Is the Corpus Luteum?

The corpus luteum is a vascular-rich glandular structure that is rapidly transformed from follicles after ovulation.

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Regulating mechanism of luteinogenesis and atrophy is an important aspect of reproduction research, but no significant progress has been made so far.

Animal experiments have shown that urokinase-type plasminogen activating factor (uPA) may have an important relationship with luteinogenesis, while tissue-type plasminogen activating factor (tPA) has an important relationship with luteal atrophy. (Liu YX, 1995; 1999).

To confirm the direct effect of tPA on luteal atrophy, the effects of tPA and uPA antibodies on the secretion of progesterone from rat and rhesus corpus luteum (CL) were observed in vitro. Adding tPA to the culture medium can reduce CL cell progesterone by 54%. Conversely, adding tPA mAb to neutralize endogenously produced tPA will increase CL secretion by 100%. This effect was also confirmed in experiments with rhesus monkeys. In contrast, uPA has no effect on the ability of CL cells to synthesize, suggesting that uPA may only play an important role in angiogenesis at the beginning of luteal formation (Liu Kui, 1997).

It has been shown that PRL and LH have a synergistic effect on the maintenance of luteal function in rats. Whether LH can inhibit tPA and stimulate progesterone production in cultured rhesus CL cells. The synergistic effect of the two hormones can further increase the production of progesterone and completely inhibit the synthesis of tPA without any significant effect on uPA. In addition to progesterone, the corpus luteum also secretes other steroid hormones and various peptide luteinizing factors. They can regulate luteal function as paracrine or autocrine factors. Further experiments have shown that interferon and tumor necrosis factor TNF can significantly stimulate tPA production in addition to inhibiting progesterone secretion (Liu YX, 1995). But its mechanism of action is unclear. Recent studies have proved that steroid synthesis sensitive regulatory protein (StAR) is an important functional indicator of the corpus luteum, and IFN and TNF also significantly inhibit the expression of StAR. Heat shock protein 70 (HSP70) expression suddenly increases during luteal atrophy, and can inhibit StAR expression and CL progesterone production. In addition to the PAPAI1 system, cytokines, PGF2, PDF70, inhibin and activin, affect StAR expression through autocrine and paracrine effects, and are important mechanisms for regulating luteal atrophy. ^[1]