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• W2518453429 abstract "The corpus luteum (CL) is a transient endocrine gland responsible for the synthesis of progesterone (P4) during the luteal phase of the menstrual cycle and early pregnancy. Timely regression of the CL (luteolysis) at the end of non-fertile cycles is necessary to allow the initiation of the next ovarian cycle, while luteolysis must be prevented if conception occurs. Therefore, understanding the factors controlling luteolysis is of considerable importance. The first event in luteolysis is a decrease in P4 synthesis (functional regression), which is then followed by the degradation and structural remodeling of the CL (structural regression). However, the molecular processes responsible for initiation of functional regression and subsequent structural regression in the primate CL are poorly defined. Therefore, a DNA microarray approach was used to systematically identify genes in the regressing rhesus macaque CL that are differentially expressed through the period of diminishing luteal P4 synthesis. CL were collected just prior to (days 10-11 post-LH surge, mid-late stage) or during (days 14-16 post-LH surge, late stage) functional regression. Based on P4 levels, late stage CL were divided into non-regressed (P4 >1.5 ng/ml) and functionally-regressed (P4 <0.5 ng/ml) groups (n=4 CL/group). Total RNA was isolated, labeled, and hybridized to Affymetrix Rhesus Macaque Total Genome Arrays. The resultant microarray data revealed that the loss of P4 synthesis in the functionally regressed CL is associated with a significant increase (>2-fold, p<0.05) in the mRNA levels of two ATP-binding cassette (ABC) transporters (ABCA1 and ABCG1) that actively transport cholesterol out of cells, a process referred to as reverse cholesterol transport. Significant decreases (>2-fold, p<0.05) in mRNA levels of genes encoding proteins responsible for extracellular cholesterol uptake, including the low-density lipoprotein receptor (LDLR) and scavenger receptor type B class 1 (SCARB1), were also noted in the regressed late stage CL (low P4) relative to the functional late stage CL (high P4) and the mid-late stage CL (high P4). The changes in mRNA levels detected by microarray were confirmed by quantitative real-time PCR. With the exception of ABCG1, a corresponding significant change (>2-fold, p<0.05) in protein levels of ABCA1, LDLR, and SCARB1 was determined by Western blot analysis. These findings indicate that there is an induction of an active cholesterol efflux system that serves to limit the steroidogenic potential of the functionally regressing macaque CL. Further support of this hypothesis came from Western blot data demonstrating that the liver X receptors α (NR1H3) and β (NR1H2), steroid hormone receptor family members that are known to stimulate expression of reverse cholesterol transport system-related genes, are expressed in the macaque CL. Furthermore, a significant increase in NR1H3 protein occurred from the mid-late to late stages of the luteal phase just prior to the drop in P4 production (>3-fold, p<0.05). Thus, these results support the hypothesis that one or both liver X receptor family members are responsible for the induction of a transport system that shuttles cholesterol out of the macaque CL, which in turn, effectively reduces luteal P4 synthesis. This research was supported by the following grants: HD42000 (JDH), HD55744 (JDH), RR00163 (JDH), and HD007133 (RLB)." @default.
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• W2518453429 date "2008-05-01" @default.
• W2518453429 modified "2023-09-23" @default.
• W2518453429 title "The Reverse Cholesterol Transport System as a Potential Mediator of Luteolysis in the Primate Corpus Luteum." @default.
• W2518453429 doi "https://doi.org/10.1093/biolreprod/78.s1.70c" @default.
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