miR-128-3p regulates chicken granulosa cell function via 14-3-3β/FoxO and PPAR-γ/LPL signaling pathways

Ning, Zifan; Deng, Xun; Li, Liang; Feng, Jing; Du, Xiaxia; Amevor, Felix Kwame; Tian, Yaofu; Li, Lingxiang; Rao, Yong; Zhang, Yi; Du, Xiaohui; Cui, Zhifu; Zhao, Xiaoling

doi:10.1016/j.ijbiomac.2023.124654

Cited by 7 publications

(4 citation statements)

References 55 publications

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“…MiR-128-3p regulates cell proliferation and apoptosis in various tissues. In this study, miR-128-3p can inhibit the proliferation of KGN cells and promote apoptosis, which is consistent with the results reported by Ning Z. et al, who observed that miR-128-3p inhibited the proliferation and promoted the apoptosis of chicken primary GCs [ 46 ]. Furthermore, the inhibition of miR-128-3p in rats can alleviate the adrenaline-induced apoptosis of GCs [ 47 ].…”

Section: Discussionsupporting

confidence: 92%

miR-128-3p Regulates Follicular Granulosa Cell Proliferation and Apoptosis by Targeting the Growth Hormone Secretagogue Receptor

Dong,

Jiang,

Hou

et al. 2024

IJMS

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The proliferation and apoptosis of granulosa cells (GCs) affect follicle development and reproductive disorders, with microRNAs playing a crucial regulatory role. Previous studies have shown the differential expression of miR-128-3p at different stages of goat follicle development, which suggests its potential regulatory role in follicle development. In this study, through the Cell Counting Kit-8 assay, the EDU assay, flow cytometry, quantitative real-time polymerase chain reaction, Western blot, and the dual-luciferase reporter assay, we used immortal human ovarian granulosa tumor cell line (KGN) cells as materials to investigate the effects of miR-128-3p and its predicted target gene growth hormone secretagogue receptor (GHSR) on GC proliferation and apoptosis. The results show that overexpression of miR-128-3p inhibited the proliferation of KGN cells, promoted cell apoptosis, and suppressed the expression of proliferating cell nuclear antigen (PCNA) and B-cell lymphoma-2 (BCL2) while promoting that of Bcl-2 associated X protein (BAX). The dual-luciferase reporter assay revealed that miR-128-3p bound to the 3′ untranslated region sequence of GHSR, which resulted in the inhibited expression of GHSR protein. Investigation of the effects of GHSR on GC proliferation and apoptosis revealed that GHSR overexpression promoted the expression of PCNA and BCL2, enhanced GC proliferation, and inhibited cell apoptosis, whereas the opposite effects were observed when GHSR expression was inhibited. In addition, miR-128-3p and GHSR can influence the expression of extracellular signal-regulated kinase 1/2 protein. In conclusion, miR-128-3p inhibits KGN cell proliferation and promotes cell apoptosis by downregulating the expression of the GHSR gene.

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Section: Discussionsupporting

confidence: 92%

miR-128-3p Regulates Follicular Granulosa Cell Proliferation and Apoptosis by Targeting the Growth Hormone Secretagogue Receptor

Dong,

Jiang,

Hou

et al. 2024

IJMS

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“…79,86 PPARG participates in lipid metabolism, estradiol and progesterone synthesis, and cell apoptosis. 87,88 Previous studies suggested that granulosa cells expressed AR, and could receive androgen and AR signaling regulation. 89 In the present study, the results of the co-culture experiments showed that compared to a single hyperandrogenic environment, the transcript levels of functional genes, IGF1, WT1, FOXO1, GATA6, and PPARG, were significantly decreased in granulosa cells in the presence of macrophages in a hyperandrogenic environment, the protein levels of CYP19a and FSHR were significantly reduced, granulosa cells were blocked in the G2-M phase and proliferation was inhibited, while the proinflammatory cytokine TNF-α was significantly elevated in the cell culture medium.…”

Section: Discussionmentioning

confidence: 99%

Hyperandrogenic environment regulates the function of ovarian granulosa cells by modulating macrophage polarization in PCOS

Chen,

Hong,

Diao

et al. 2024

American J Rep Immunol

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BackgroundPolycystic ovary syndrome (PCOS) is a common endocrine‐metabolic disorder characterized by oligo‐anovulation, hyperandrogenism, and polycystic ovaries, with hyperandrogenism being the most prominent feature of PCOS patients. However, whether excessive androgens also exist in the ovarian microenvironment of patients with PCOS, and their modulatory role on ovarian immune homeostasis and ovarian function, is not clear.MethodsFollicular fluid samples from patients participating in their first in vitro fertilization/intracytoplasmic sperm injection (IVF/ICSI) treatment were collected. Androgen concentration of follicular fluid was assayed by chemiluminescence, and the macrophage M1:M2 ratio was detected by flow cytometry. In an in vitro model, we examined the regulatory effects of different concentrations of androgen on macrophage differentiation and glucose metabolism levels using qRT‐PCR, Simple Western and multi‐factor flow cytometry assay. In a co‐culture model, we assessed the effect of a hyperandrogenic environment in the presence or absence of macrophages on the function of granulosa cells using qRT‐PCR, Simple Western, EdU assay, cell cycle assay, and multi‐factor flow cytometry assay.ResultsThe results showed that a significantly higher androgen level and M1:M2 ratio in the follicular fluid of PCOS patients with hyperandrogenism. The hyperandrogenic environment promoted the expression of pro‐inflammatory and glycolysis‐related molecules and inhibited the expression of anti‐inflammatory and oxidative phosphorylation‐related molecules in macrophages. In the presence of macrophages, a hyperandrogenic environment significantly downregulated the function of granulosa cells.ConclusionThere is a hyperandrogenic microenvironment in the ovary of PCOS patients with hyperandrogenism. Hyperandrogenic microenvironment can promote the activation of ovarian macrophages to M1, which may be associated with the reprogramming of macrophage glucose metabolism. The increased secretion of pro‐inflammatory cytokines by macrophages in the hyperandrogenic microenvironment would impair the normal function of granulosa cells and interfere with normal ovarian follicle growth and development.

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“…Studies have shown that adipose tissue regulates fat metabolism by secreting CAMs [ 51 , 52 ]. The ECM–receptor pathway regulates adipocyte development and function by modulating intracellular signaling pathways, forming and maintaining the structure of adipose tissue, and modulating lipid deposition [ 51 , 52 ], whereas the PPAR pathway is associated with regulating lipid metabolism [ 53 , 54 ].…”

Section: Discussionmentioning

confidence: 99%

RNA-Seq Analysis Reveals the Molecular Mechanisms Regulating the Development of Different Adipose Tissues in Broiler Chicks

Wei,

Kang,

Amevor

et al. 2024

Animals

Self Cite

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In an effort to enhance growth rates, chicken breeders have undertaken intensive genetic selection. In the selection process, the primary aim is to accelerate growth, inadvertently leading to new chicken breeds having an increased capacity for rapid adipose tissue accumulation. However, little is known about the relationship between changes in gene expression and adipose tissue accumulation and deposition in chickens. Therefore, in this study, RNA-seq analysis was utilized, and transcriptome data were obtained from the abdominal fat, thoracic subcutaneous fat, and clavicular fat on day 1 (d1), day 4, day 7, day 11, and day 15 to reveal the molecular mechanisms regulating the development and deposition of different adipose tissues in broiler chicks. The results showed that the key period for adipocyte differentiation and proliferation was between d4 and d7 (abdominal fat development) and between d1 and d4 (chest subcutaneous fat and clavicular fat). In addition, candidate genes such as MYOG, S100A9, CIDEC, THRSP, CXCL13, and NMU related to adipose tissue growth and development were identified. Further, genes (HOXC9, AGT, TMEM182, ANGPTL3, CRP, and DSG2) associated with the distribution of adipose tissue were identified, and genes (MN1, ANK2, and CAP2) related to adipose tissue growth were also identified. Taken together, the results from this study provide the basis for future studies on the mechanisms regulating adipose tissue development in chickens. Further, the candidate genes identified could be used in the selection process.

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miR-128-3p regulates chicken granulosa cell function via 14-3-3β/FoxO and PPAR-γ/LPL signaling pathways

Cited by 7 publications

References 55 publications

miR-128-3p Regulates Follicular Granulosa Cell Proliferation and Apoptosis by Targeting the Growth Hormone Secretagogue Receptor

miR-128-3p Regulates Follicular Granulosa Cell Proliferation and Apoptosis by Targeting the Growth Hormone Secretagogue Receptor

Hyperandrogenic environment regulates the function of ovarian granulosa cells by modulating macrophage polarization in PCOS

RNA-Seq Analysis Reveals the Molecular Mechanisms Regulating the Development of Different Adipose Tissues in Broiler Chicks

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