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Title 

Progesterone production is affected by unfolded protein response (UPR) signaling during the luteal phase in mice

Authors 

H J ParkS J ParkD B KooSang-Rae LeeI K KongJ W RyooY I ParkKyu Tae ChangD S Lee

Publisher 

Elsevier

Issue Date 

2014

Citation 

Life Sciences, vol. 113, no. 1, pp. 60-67

Keywords 

Corpus luteumER stressLuteal phaseProgesterone productionUnfolded protein response

Abstract 

Aims: We examined whether the three unfolded protein response (UPR) signaling pathways, which are activated in response to endoplasmic reticulum (ER)-stress, are involved in progesterone production in the luteal cells of the corpus luteum (CL) during the mouse estrous cycle. Main methods: The luteal phase of C57BL/6 female mice (8 weeks old) was divided into two stages: the functional stage (16, 24, and 48 h) and the regression stage (72 and 96 h). Western blotting and reverse transcription (RT)-PCR were performed to analyze UPR protein/gene expression levels in each stage. We investigated whether ER stress affects the progesterone production by using Tm (0.5 μg/g. BW) or TUDCA (0.5 μg/g. BW) through intra-peritoneal injection. Key findings: Our results indicate that expressions of Grp78/Bip, p-eIF2α/ATF4, p50ATF6, and p-IRE1/sXBP1 induced by UPR activation were predominantly maintained in functional and early regression stages of the CL. Furthermore, the expression of p-JNK, CHOP, and cleaved caspase3 as ER-stress mediated apoptotic factors increased during the regression stage. Cleaved caspase3 levels increased in the late-regression stage after p-JNK and CHOP expression in the early-regression stage. Additionally, although progesterone secretion and levels of steroidogenic enzymes decreased following intra-peritoneal injection of Tunicamycin, an ER stress inducer, the expression of Grp78/Bip, p50ATF6, and CHOP dramatically increased. Significance: These results suggest that the UPR signaling pathways activated in response to ER stress may play important roles in the regulation of the CL function. Furthermore, our findings enhance the understanding of the basic mechanisms affecting the CL life span.

ISSN 

0024-3205

Link 

http://dx.doi.org/10.1016/j.lfs.2014.07.033

Appears in Collections

1. Journal Articles > Journal Articles

Registered Date

2019-05-02


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