Related Experiment Video

Updated: Oct 7, 2025

Mechanism of Kemeng Fang's Inhibition of Podocyte Apoptosis in Rats with Membranous Nephropathy through the PI3K/AKT Signaling Pathway
07:15

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

565

Leukemia inhibitory factor prevents chicken follicular atresia through PI3K/AKT and Stat3 signaling pathways

Juan Dong1, Changquan Guo1, Shuo Zhou1

  • 1Department of Veterinary Medicine, College of Animal Sciences, Zhejiang University, Hangzhou, 310058, China.

Molecular and Cellular Endocrinology
|January 6, 2022
PubMed

Insights

Leukemia inhibitory factor (LIF) prevents chicken follicular atresia by inhibiting granulosa cell autophagic apoptosis via PI3K/AKT and Stat3 pathways. This promotes follicle development and alleviates cell death.

Area of Science:

  • Reproductive Biology
  • Cellular Biology
  • Endocrinology

Background:

  • Autophagy in granulosa cells (GCs) contributes to follicular atresia, a process linked with apoptosis.
  • Leukemia inhibitory factor (LIF) promotes follicular growth, but its molecular mechanisms are not fully understood.

Purpose of the Study:

  • To elucidate the role of LIF in regulating granulosa cell autophagy and apoptosis during chicken follicular atresia.
  • To investigate the signaling pathways involved in LIF's protective effects on follicular development.

Main Methods:

  • Administration of rapamycin (autophagy inducer) and LIF to chicken follicles.
  • Assessment of granulosa cell viability, apoptosis, and autophagy.
  • Analysis of key signaling pathway activation (PI3K/AKT, Stat3) and protein expression (BCL-2, BECN1).
  • Inhibition of PI3K/AKT and Stat3 pathways to evaluate LIF's protective function.

Main Results:

  • Rapamycin induced GC apoptosis and inhibited follicular growth.
  • Combined LIF treatment alleviated rapamycin-induced follicular regression by enhancing GC viability and reducing autophagic apoptosis.
  • LIF activated PI3K/AKT and Stat3 pathways, increasing BCL-2 and decreasing BECN1 expression.
  • Blocking PI3K/AKT and Stat3 pathways diminished LIF's protective effect against follicular atresia.

Conclusions:

  • LIF inhibits granulosa cell autophagic cell death by activating PI3K/AKT and Stat3 signaling pathways.
  • LIF effectively alleviates chicken follicular atresia, offering a potential therapeutic target for reproductive health.
Keywords:
ApoptosisAutophagyChickenFollicular atresiaLeukemia inhibitory factor

More Related Videos

Proliferation and Differentiation of Murine Myeloid Precursor 32D/G-CSF-R Cells10:21

Proliferation and Differentiation of Murine Myeloid Precursor 32D/G-CSF-R Cells

Published on: February 21, 2018

10.1K
Cancer-Associated Fibroblasts from Mouse Mammary Tumors as Tools for Molecular and Computational Studies09:01

Cancer-Associated Fibroblasts from Mouse Mammary Tumors as Tools for Molecular and Computational Studies

Published on: July 3, 2025

328

Related Concept Videos

The JAK-STAT Signaling Pathway01:20

The JAK-STAT Signaling Pathway

Several cytokine receptors have tightly bound Janus kinase or JAK proteins attached at their cytosolic tail. Small signaling molecules such as cytokines, growth hormones, or prolactins bind to the cytokine receptors and initiate their dimerization. The dimerization brings the cytosolic JAKs together that trans-phosphorylate and activates each other. The activated JAKs now phosphorylate cytosolic tails of the cytokine receptors, which serve as binding sites for adaptor proteins such as  SH2...
9.5K
The Intrinsic Apoptotic Pathway01:31

The Intrinsic Apoptotic Pathway

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...
7.0K
PI3K/mTOR/AKT Signaling Pathway01:22

PI3K/mTOR/AKT Signaling Pathway

The mammalian target of rapamycin  (mTOR) is a serine/threonine kinase that regulates growth, proliferation, and cell survival in response to hormones, growth factors, or nutrient availability. This kinase exists in two structurally and functionally distinct forms: mTOR complex 1  (mTORC1) and mTOR complex 2  (mTORC2). The first form (mTORC1) is composed of a rapamycin-sensitive Raptor and proline-rich Akt substrate, PRAS40. In contrast,  mTORC2 consists of a...
4.1K
Regulation of Angiogenesis and Blood Supply01:24

Regulation of Angiogenesis and Blood Supply

Rapidly dividing tumors, embryos, and wounded tissues require more oxygen than usual, lowering the oxygen concentration in the blood. At low oxygen or hypoxic conditions, an oxygen-sensitive transcription factor called the hypoxia-inducible factor 1 or HIF1 is activated. HIF1 is a dimeric protein of alpha (ɑ) and beta (β) subunits.  Under optimal oxygen conditions, HIF1β is present in the nucleus while HIF1ɑ remains in the cytosol. HIF1ɑ is hydroxylated by prolyl...
2.8K
Inhibition of Cdk Activity02:34

Inhibition of Cdk Activity

The orderly progression of the cell cycle depends on the activation of Cdk protein by binding to its cyclin partner. However, the cell cycle must be restricted when undergoing abnormal changes. Most cancers correlate to the deregulated cell cycle, and since Cdks are a central component of the cell cycle, Cdk inhibitors are extensively studied to develop anticancer agents. For instance, cyclin D associates with several Cdks, such as Cdk 4/6, to form an active complex. The cyclin D-Cdk4/6 complex...
5.0K
Role Of Notch Signalling In Intestinal Stem Cell Renewal01:12

Role Of Notch Signalling In Intestinal Stem Cell Renewal

Notch signaling was first discovered in Drosophila melanogaster, where it is involved in cell lineage differentiation. Notch signaling regulates the maintenance and differentiation of intestinal stem cells or ISCs by controlling the expression of atonal homolog 1 or Atoh1. Atoh1 directs cells to differentiate into secretory cells.
Direct cell-to-cell contact is needed for the activation of Notch signaling. The signal is initiated when a notch ligand binds to a receptor on an adjacent cell, also...
2.2K