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Related Concept Videos

NF-κB-dependent Signaling Pathway02:26

NF-κB-dependent Signaling Pathway

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The transcription factor NF-κB was discovered in 1986 in the lab of Nobel laureate Professor David Baltimore, for its interaction with the immunoglobulin light chain enhancer in B-cells. After more than three decades of study, it is now evident that NF-κB regulates the expression of over 100 genes. Most of these genes play an essential role in the innate and adaptive immune responses as well as the inflammatory responses of animals.
NF-κB-dependent Signaling Mechanism
The...
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Feedback Regulation of Calcium Concentration01:27

Feedback Regulation of Calcium Concentration

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Calcium is an essential signaling molecule required for various cellular functions. Calcium pumps and ion channels on cell and organellar membranes, such as those on the endoplasmic reticulum (ER), regulate calcium concentrations inside the cell. They remain closed, keeping the cytosolic calcium levels low at a resting state.
Various transmembrane receptors, such as G protein-coupled receptors (GPCRs), elicit a response to extracellular signals by increasing cytosolic calcium. Activated GPCRs...
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The Intrinsic Apoptotic Pathway01:31

The Intrinsic Apoptotic Pathway

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Internal cellular stress, such as cellular injury or hypoxia, triggers intrinsic apoptosis. The B-cell lymphoma 2 (Bcl-2) family of proteins are the primary regulators of the intrinsic apoptotic pathway. For example, during DNA damage, checkpoint proteins, such as Ataxia Telangiectasia Mutated (ATM protein) and Checkpoints Factor-2 (Chk2) proteins, are activated. These proteins phosphorylate p53 which further activates pro-apoptotic proteins, such as Bax, Bak, PUMA, and Noxa, and inhibits...
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TGF - β Signaling Pathway01:16

TGF - β Signaling Pathway

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The TGF-β signaling pathway regulates cell growth, differentiation, adhesion, motility, and development. TGF-β ligands that induce TGF-β signaling are synthesized in their latent form. Several proteases or cell surface receptors such as integrins act upon the latent form, releasing the active ligand. There are three types of mammalian TGF-βs: (TGF-β1, TGF-β2, and TGF-β3) that bind as homodimers or heterodimers to TGF-β receptors. The TGF-β receptors...
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The Extrinsic Apoptotic Pathway01:17

The Extrinsic Apoptotic Pathway

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The extrinsic apoptotic pathway is initiated when extracellular death-inducing signals, such as specific cytokines, activate the death receptors expressed on the cell surface. The immune cells involved in this pathway are natural killer cells (NK cells) and cytotoxic T-lymphocytes. NK cells are critical in innate immune response, while cytotoxic T-lymphocytes are associated with adaptive immune response. These cells recognize specific receptors expressed on the altered cells and activate...
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Negative Regulator Molecules01:23

Negative Regulator Molecules

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Positive regulators allow a cell to advance through cell cycle checkpoints. Negative regulators have an equally important role as they terminate a cell’s progression through the cell cycle—or pause it—until the cell meets specific criteria.
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  1. Home
  3. Research Domains
  5. Biomedical And Clinical Sciences
  7. Oncology And Carcinogenesis
  9. Predictive And Prognostic Markers
  11. The Mechanism Of Nf-κb-tert Feedback Regulation Of Granulosa Cell Apoptosis In Pcos Rats.
  1. Home
  3. Research Domains
  5. Biomedical And Clinical Sciences
  7. Oncology And Carcinogenesis
  9. Predictive And Prognostic Markers
  11. The Mechanism Of Nf-κb-tert Feedback Regulation Of Granulosa Cell Apoptosis In Pcos Rats.

Related Experiment Video

Mechanism of Kemeng Fang's Inhibition of Podocyte Apoptosis in Rats with Membranous Nephropathy through the PI3K/AKT Signaling Pathway
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Mechanism of Kemeng Fang's Inhibition of Podocyte Apoptosis in Rats with Membranous Nephropathy through the PI3K/AKT Signaling Pathway

Published on: August 23, 2024

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The mechanism of NF-κB-TERT feedback regulation of granulosa cell apoptosis in PCOS rats.

Haoxuan Xue1, Zecheng Hu2, Shun Liu1

  • 1The First Affiliated Hospital, Gynecology & Obstetrics and Reproductive Medical Center, Clinical Anatomy and Reproductive Medicine Application Institute, School of Basic Medical Sciences, Hengyang Medical School, University of South China, Hengyang, Hunan, China.

Plos One
|October 25, 2024

View abstract on PubMed

Summary
This summary is machine-generated.

Polycystic ovary syndrome (PCOS) involves ovarian inflammation. Nuclear factor kappa-B (NF-κB) and Telomerase reverse transcriptase (TERT) may drive granulosa cell apoptosis in PCOS via inflammatory pathways.

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Methods for the Modulation and Analysis of NF-κB-dependent Adult Neurogenesis
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A Tissue Culture Model of Estrogen-producing Primary Bovine Granulosa Cells
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A Tissue Culture Model of Estrogen-producing Primary Bovine Granulosa Cells

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Mechanism of Kemeng Fang's Inhibition of Podocyte Apoptosis in Rats with Membranous Nephropathy through the PI3K/AKT Signaling Pathway
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Methods for the Modulation and Analysis of NF-κB-dependent Adult Neurogenesis
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A Tissue Culture Model of Estrogen-producing Primary Bovine Granulosa Cells
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A Tissue Culture Model of Estrogen-producing Primary Bovine Granulosa Cells

Published on: September 6, 2018

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Area of Science:

  • Reproductive Endocrinology
  • Cell Biology
  • Molecular Medicine

Background:

  • Polycystic ovary syndrome (PCOS) is characterized by chronic low-grade ovarian inflammation.
  • Inflammation and telomere dysfunction are linked, but the feedback mechanisms between inflammatory signaling and telomere-telomerase regulation in PCOS remain unclear.

Purpose of the Study:

  • To investigate the role of the Nuclear factor kappa-B (NF-κB) and Telomerase reverse transcriptase (TERT) feedback loop in PCOS granulosa cell apoptosis.
  • To elucidate the molecular mechanisms underlying chronic inflammation in PCOS.

Main Methods:

  • Established PCOS rat models using letrozole and a high-fat diet.
  • Utilized a Lipopolysaccharide (LPS)-induced KGN cell inflammation model.
  • Administered NF-κB and TERT inhibitors (BAY 11-7082 and BIBR1532) to LPS-treated KGN cells.

Main Results:

  • PCOS rats exhibited hormonal imbalances, ovarian morphology changes, and increased expression of NF-κB, IL-6, TNF-α, TERT, Bax, and Caspase-3, with decreased Bcl-2 and telomere elongation.
  • LPS-treated KGN cells showed elevated inflammatory and pro-apoptotic markers, which were reversed by NF-κB and TERT inhibitor treatment.
  • Significant positive correlations were found between NF-κB, inflammatory factors, TERT, and pro-apoptotic markers (Bax, Caspase-3), and negative correlation with Bcl-2.

Conclusions:

  • Telomerase reverse transcriptase (TERT) may induce granulosa cell apoptosis by modulating the NF-κB signaling pathway.
  • This interaction contributes to the chronic inflammatory response in PCOS, mediated by downstream factors like IL-6 and TNF-α.