The expression of autophagy-related proteins within the corpus luteum lifespan in pigs

Grzesiak, Małgorzata; Michalik, Anna; Rak, Agnieszka; Knapczyk-Stwora, Katarzyna; Pieczonka, Anna

doi:10.1016/j.domaniend.2018.03.004

Cited by 21 publications

(14 citation statements)

References 28 publications

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“…Consistent with this, we found a high expression of the pro-apoptotic factor cleaved Caspase3 in the late stages of the luteal phase of the goat CL, suggesting that UPR may be involved in goat luteal cell apoptosis, as UPR was also activated in the late stages of the luteal phase. We also detected an increased level of autophagy in the late stages of the luteal phase of the goat CL, which is similar to a previous report that autophagy occurs in luteal cells during CL regression ( Choi et al, 2014 ; Aboelenain et al, 2015 ; Grzesiak et al, 2018 ). This suggests that both autophagy and UPR are involved in CL regression, and we predict that both autophagy and UPR regulate luteal cell apoptosis in the late luteal phase of goat CL.…”

Section: Discussionsupporting

confidence: 91%

Prostaglandin F2α Induces Goat Corpus Luteum Regression via Endoplasmic Reticulum Stress and Autophagy

Wen

Liu

et al. 2020

Front. Physiol.

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Corpus luteum (CL) is a transient endocrine tissue that produces progesterone for maintaining pregnancy in mammals. In addition, the regression of CL is necessary for the initiation of the estrous cycle. Extensive research has shown that the prostaglandin F2α (PGF2α) induces the regression of CL in ruminants. However, the mechanisms of endoplasmic reticulum (ER) stress and autophagy in the regression of goat CL induced by PGF2α are still unclear. In this study, ovaries of dioestrus goats and goats that were 3 months pregnant were collected to detect the location of the ER stress-related protein GRP78. The relationship between the different stages of the luteal phase of goat CL during the estrous cycle and changes in the expression of ER stress-related proteins and autophagy-related proteins was confirmed by western blot analysis. The results showed that both ER stress and autophagy were activated in the late luteal phase of the goat CL. To reveal the function of ER stress and autophagy in the CL regression process induced by PGF2α, we used 4-phenyl butyric acid (4-PBA) and chloroquine (CQ) for inhibiting ER stress and autophagy, respectively. Through the apoptotic rate detected by the flow cytometry and the expression of ER stress-and autophagy-related proteins detected by western blotting, we demonstrated that ER stress promoted goat luteal cell apoptosis and autophagy, and that apoptosis can be enhanced by the inhibition of autophagy. In addition, knockdown of EIF2S1, which blocked the PERK pathway activation, promoted apoptosis by reducing autophagy in goat luteal cells treated with PGF2α. In conclusion, our study indicates that ER stress promotes goat luteal cell apoptosis to regulate the regression of CL and activates autophagy to inhibit the goat luteal cell apoptosis via PERK signaling pathway.

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Section: Discussionsupporting

confidence: 91%

Prostaglandin F2α Induces Goat Corpus Luteum Regression via Endoplasmic Reticulum Stress and Autophagy

Wen

Liu

et al. 2020

Front. Physiol.

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“…In the ovary, autophagy has been associated with follicle development and atresia as well as luteal formation and regression [ 174 , 176 , 214 , 215 , 216 , 217 , 218 , 219 ]. Recently, Tang et al (2020) found that HIF1α enhances autophagy in the rat luteinized granulosa cells [ 217 ].…”

Section: Metabolic Events Induced By Lh In the Corpus Luteum: The Crosstalk Of Pka/mtor And Ampk Signaling In The Regulation Of Metabolicmentioning

confidence: 99%

“…These findings are correlated with studies showing enhanced activity of lysosomes and decreased expression of MTOR in the late corpus luteum [ 176 ]. In the pig, the expression of Beclin1 and LAMP1, proteins specific for autophagosomes and lysosomes, respectively, was highest in the corpus luteum during late luteal phase [ 215 ]. Our recent data showed elevated content of LC3B in the luteal tissue during induced luteolysis [ 222 ].…”

Section: Metabolic Events Induced By Lh In the Corpus Luteum: The Crosstalk Of Pka/mtor And Ampk Signaling In The Regulation Of Metabolicmentioning

confidence: 99%

Luteinizing Hormone Regulation of Inter-Organelle Communication and Fate of the Corpus Luteum

Przygrodzka

Plewes

Davis

2021

IJMS

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The corpus luteum is an endocrine gland that synthesizes the steroid hormone progesterone. luteinizing hormone (LH) is a key luteotropic hormone that stimulates ovulation, luteal development, progesterone biosynthesis, and maintenance of the corpus luteum. Luteotropic and luteolytic factors precisely regulate luteal structure and function; yet, despite recent scientific progress within the past few years, the exact mechanisms remain largely unknown. In the present review, we summarize the recent progress towards understanding cellular changes induced by LH in steroidogenic luteal cells. Herein, we will focus on the effects of LH on inter-organelle communication and steroid biosynthesis, and how LH regulates key protein kinases (i.e., AMPK and MTOR) responsible for controlling steroidogenesis and autophagy in luteal cells.

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“…In fact, expression of various autophagy related factors is increased in the late luteal and regression stages of the CL. Increased expression of beclin protein during the late luteal stage in the sow suggests a role in the removal of unwanted proteins during luteolysis (78). LC3-II, an autophagy marker is expressed more in the late than middle stage CL in cattle (42).…”

Section: Autophagy and CL Regressionmentioning

confidence: 99%

Possible Mechanisms for Maintenance and Regression of Corpus Luteum Through the Ubiquitin-Proteasome and Autophagy System Regulated by Transcriptional Factors

et al. 2019

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The corpus luteum (CL) is an important tissue of the female reproductive process which is established through ovulation of the mature follicle. Pulsatile release of prostaglandin F2α from the uterus leads to the regression of luteal cells and restarts the estrous cycle in most non-primate species. The rapid functional regression of the CL, which coincides with decrease of progesterone production, is followed by its structural regression. Although we now have a better understanding of how the CL is triggered to undergo programmed cell death, the precise mechanisms governing CL protein degradation in a very short period of luteolysis remains unknown. In this context, activation of ubiquitin-proteasome pathway (UPP), unfolded protein response (UPR) and autophagy are potential subcellular mechanisms involved. The ubiquitin-proteasome pathway (UPP) maintains tissue homeostasis in the face of both internal and external stressors. The UPP also controls physiological processes in many gonadal cells. Emerging evidence suggests that UPP dysfunction is involved in male and female reproductive tract dysfunction. Autophagy is activated when cells are exposed to different types of stressors such as hypoxia, starvation, and oxidative stress. While emerging evidence points to an important role for the UPP and autophagy in the CL, the key underlying transcriptional mechanisms have not been well-documented. In this review, we propose how CL regression may be governed by the ubiquitin-proteasome and autophagy pathways. We will further consider potential transcription factors which may regulate these events in the CL.

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The expression of autophagy-related proteins within the corpus luteum lifespan in pigs

Cited by 21 publications

References 28 publications

Prostaglandin F2α Induces Goat Corpus Luteum Regression via Endoplasmic Reticulum Stress and Autophagy

Prostaglandin F2α Induces Goat Corpus Luteum Regression via Endoplasmic Reticulum Stress and Autophagy

Luteinizing Hormone Regulation of Inter-Organelle Communication and Fate of the Corpus Luteum

Possible Mechanisms for Maintenance and Regression of Corpus Luteum Through the Ubiquitin-Proteasome and Autophagy System Regulated by Transcriptional Factors

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