Expression of PUMA in Follicular Granulosa Cells Regulated by FoxO1 Activation During Oxidative Stress

Liu, Zequn; Shen, Ming; Wu, Wangjun; Li, Bo-jiang; Weng, Qiannan; Li, Mei; Liu, Honglin

doi:10.1177/1933719114556483

Cited by 41 publications

(34 citation statements)

References 45 publications

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“…In the present study, bGCs were exposed to different levels of in-vitro heat stress and found that heat stress involves compromising the physiological functions of bGCs by increasing intracellular accumulation of ROS, inducing apoptosis and reducing the synthesis of E2 and P4 [7,9,15]. For more understanding, we conducted the transcriptomic study of in-vitro cultured bGCs exposed to heat stress at 39, 40, and 41°C.…”

Section: Discussionmentioning

confidence: 90%

“…Heat shock 70 kDa protein (HSP70) is a major stress protein induced in mouse GCs by high temperature [9]. Increasing evidence suggests that heat stress induces intracellular ROS concentration [14], resulting in apoptosis of granulosa cells in the mouse [15]. In addition, ROS may subsequently alter the development of bovine embryos during in-vitro oocyte maturation [16].…”

Section: Introductionmentioning

confidence: 99%

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Evaluation of heat stress effects on cellular and transcriptional adaptation of bovine granulosa cells

Khan

Dou

Wang

et al. 2020

J Animal Sci Biotechnol

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Background: Heat stress is known to affect follicular dynamics, oocyte maturation, and fertilization by impairing steroidogenic ability and viability of bovine granulosa cell (bGCs). The present study explored the physiological and molecular response of bGCs to different heat stress intensities in-vitro. We exposed the primary bGCs to heat stress (HS) at 39°C, 40°C and 41°C along with control samples (38°C) for 2 h. To evaluate the impact of heat stress on bGCs, several in vitro cellular parameters including cell apoptosis, intracellular reactive oxygen species (ROS) accumulation and HSP70 kinetics were assessed by flow cytometry, florescence microscopy and western blot, respectively. Furthermore, the ELISA was performed to confirm the 17β-estradiol (E 2 ) and progesterone (P 4 ) levels. In addition, the RNA sequencing (RNA-Seq) method was used to get the molecular based response of bGCs to different heat treatments. Results: Our findings revealed that the HS significantly decreased the cell viability, E 2 and P 4 levels in bGCs, whereas, increased the cellular apoptosis and ROS. Moreover, the RNA-Seq experiments showed that all the treatments (39°C, 40°C and 41°C) significantly regulated many differentially expressed genes (DEGs) i.e. BCL2L1, STAR, CYP11A1, CASP3, SOD2, HSPA13, and MAPK8IP1 and pathways associated with heat stress, apoptosis, steroidogenesis, and oxidative stress. Conclusively, our data demonstrated that the impact of 40°C treatment was comparatively detrimental for cell viability, apoptosis and ROS accumulation. Notably, a similar trend of gene expression was reported by RT-qPCR for RNA-seq data. Conclusions:Our study presented a worthy strategy for the first time to characterize the cellular and transcriptomic adaptation of bGCs to heat stress (39, 40 and 41°C) in-vitro. The results infer that these genes and pathways reported in present study could be useful candidates/indicators for heat stress research in dairy cattle. Moreover, the established model of bGCs to heat stress in the current study provides an appropriate platform to understand the mechanism of how heat-stressed bGCs can affect the quality of oocytes and developing embryo.

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Section: Discussionmentioning

confidence: 90%

Section: Introductionmentioning

confidence: 99%

Evaluation of heat stress effects on cellular and transcriptional adaptation of bovine granulosa cells

Khan

Dou

Wang

et al. 2020

J Animal Sci Biotechnol

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“…We also detected the induction of PUMA mRNA and protein in the livers of Chrebp -/-mice fed a 34% fructose diet (Supplemental Figure 6, E and F). Meanwhile, FOXO1 and p53 protein levels were comparable between WT and Chrebp -/-livers ( Figure 1J), indicating that the induction of PUMA was probably not due to FOXO1 and p53, two known transcription activators of Puma (26,27).…”

Section: A Hfrd Activates the C/ebp Homologous Protein-mediated Apoptmentioning

confidence: 83%

Lipogenic transcription factor ChREBP mediates fructose-induced metabolic adaptations to prevent hepatotoxicity

Zhang

Tong

VanDommelen

et al. 2017

Journal of Clinical Investigation

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“…FoxO1 regulates Bim gene expression by binding to its promoter in oxidative stress-induced apoptosis [23]. Moreover, FoxO1 induces cell apoptosis via modulating Puma expression in oxidative stress-induced MGCs [24]. …”

Section: Introductionmentioning

confidence: 99%

Oxidative Stress Induces Mouse Follicular Granulosa Cells Apoptosis via JNK/FoxO1 Pathway

Weng

Liu

et al. 2016

PLoS ONE

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The c-Jun N-terminal protein kinase (JNK) plays an important role in the regulation of cell apoptosis. Forkhead box O (FoxO) transcription factors are involved in diverse biological processes, including cellular metabolism, cell apoptosis, and cell cycle. However, the JNK/FoxO1 pathway involved in the process of apoptosis induced by oxidative stress remains to be elucidated. Here, we demonstrated that the JNK activity significantly increased in response to oxidative stress in mouse follicular granulosa cells (MGCs). SP600125, a selective JNK inhibitor, attenuated the oxidative stress-induced MGCs apoptosis. Oxidative stress enhanced the FoxO1 nuclear translocation by activating the JNK activity. Moreover, JNK mediated the dissociation of FoxO1 from 14-3-3 proteins in MGCs after the treatment with H2O2. Finally, oxidative stress up-regulated the expression of FoxO1 via JNK mediation of FoxO1 self-regulation in MGCs. Taken together, our findings suggest that JNK/FoxO1 is involved in the regulation of oxidative stress-induced cell apoptosis in MGCs.

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Expression of PUMA in Follicular Granulosa Cells Regulated by FoxO1 Activation During Oxidative Stress

Cited by 41 publications

References 45 publications

Evaluation of heat stress effects on cellular and transcriptional adaptation of bovine granulosa cells

Evaluation of heat stress effects on cellular and transcriptional adaptation of bovine granulosa cells

Lipogenic transcription factor ChREBP mediates fructose-induced metabolic adaptations to prevent hepatotoxicity

Oxidative Stress Induces Mouse Follicular Granulosa Cells Apoptosis via JNK/FoxO1 Pathway

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