Peroxiredoxin I maintains luteal function by regulating unfolded protein response

Area of Science:

• Reproductive biology
• Endocrinology
• Cellular stress response

Background:

• Antioxidants regulate steroidogenesis and progesterone production in the corpus luteum (CL).
• The role of peroxiredoxin 1 (PRDX1) in CL function and progesterone synthesis remains unclear.
• This study investigates PRDX1's mechanism in maintaining luteal function and progesterone production.

Purpose of the Study:

• To evaluate the functional link between PRDX1 and progesterone production in the CL of Prdx1 knockout (K/O) mice.
• To elucidate the role of ER stress and UPR signaling in PRDX1-deficient CL.
• To determine the effects of antioxidant treatment on luteal function in Prdx1 K/O mice.

Main Methods:

• Western blotting to analyze UPR signaling, ER stress, apoptosis markers, and PRDX1 in CL tissue.
• Investigated protein levels after tunicamycin (Tm), tauroursodeoxycholic acid (TUDCA), and N-acetylcysteine (NAC) treatments in wild-type mice.
• Examined progesterone production and UPR gene expression in Prdx1 K/O mice.

Main Results:

• PRDX1 deficiency activated UPR signaling and ER stress-induced apoptosis in the CL.
• Prdx1 K/O mice exhibited decreased CL number, serum progesterone, and steroidogenic enzyme expression.
• NAC administration partially restored progesterone production and reduced ER stress markers in Prdx1 K/O mice.

Conclusions:

• PRDX1 is crucial for maintaining CL function and progesterone production in mice.
• PRDX1 deficiency leads to ER stress and UPR activation, compromising luteal function.
• These findings reveal the underlying mechanisms connecting PRDX1 to progesterone production in the CL.