Related Experiment Video

Updated: Apr 8, 2026

Trophoblast Cell Recovery from Angiogenesis-Tube Formation Assay for Differentiation Marker Expression Analysis
05:30

Trophoblast Cell Recovery from Angiogenesis-Tube Formation Assay for Differentiation Marker Expression Analysis

Published on: November 8, 2024

1.1K

PP007. Effects of STAT1 suppression on ERK1/2 in trophoblastic cells

F L P Sousa1, D M Morales Prieto2, S Ospina Prieto2

  • 1Obstetrics, Placenta-Laboratories/University Hospital Jena, Jena, Germany; Obstetrics, Federal University of São Paulo, São Paulo, Brazil.

Pregnancy Hypertension
|June 25, 2015
PubMed
Abstract

Insights

Placental cytokines activate STAT1 (signal transducer and activator of transcription 1) in trophoblast cells. Suppressing STAT1 impacts ERK1/2 (extracellular signal-regulated kinase 1/2) activity, revealing a crucial crosstalk between these pathways.

Area of Science:

  • Reproductive biology and cell signaling.
  • Investigating molecular mechanisms in trophoblast function.

Background:

  • Trophoblast cell migration and invasion are vital for pregnancy, regulated by cytokines and growth factors.
  • Key intracellular pathways, Janus kinase/signal transducer and activator of transcription (JAK-STAT) and extracellular regulated kinase1/2 (ERK1/2), influence gene expression, proliferation, and embryo development.

Purpose of the Study:

  • To characterize and analyze the regulation and crosstalk between STAT1 and ERK1/2 pathways in trophoblast cells.
  • To identify specific cytokines that activate these signaling pathways.

Main Methods:

  • Utilized HTR-8/svneo and JEG-3 trophoblast cell lines, stimulated with cytokines like LIF and OSM.
  • Analyzed STAT1 and ERK1/2 phosphorylation via Western blotting.
  • Inhibited STAT1 using fludarabine or small interfering RNA (siRNA) and assessed proliferation and invasion.

Main Results:

  • Leukemia inhibitory factor (LIF) and oncostatin M (OSM) induced STAT1 and ERK1/2 phosphorylation.
  • STAT1 suppression by fludarabine or siRNA altered ERK1/2 phosphorylation, indicating pathway crosstalk.
  • STAT1 inhibition reduced STAT1 DNA-binding capacity and slightly decreased cell invasiveness.

Conclusions:

  • STAT1 is activated by placental cytokines in trophoblast cells.
  • A significant crosstalk exists between STAT1 and ERK1/2 pathways, as evidenced by mutual influence upon suppression.
  • Further research is needed to elucidate the precise mechanisms behind the observed effects on ERK1/2 activity.

More Related Videos

Induction and Analysis of Epithelial to Mesenchymal Transition10:37

Induction and Analysis of Epithelial to Mesenchymal Transition

Published on: August 27, 2013

36.7K
Studying TGF-β Signaling and TGF-β-induced Epithelial-to-mesenchymal Transition in Breast Cancer and Normal Cells06:54

Studying TGF-β Signaling and TGF-β-induced Epithelial-to-mesenchymal Transition in Breast Cancer and Normal Cells

Published on: October 27, 2020

14.8K

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...
14.0K
Mitogens and the Cell Cycle02:38

Mitogens and the Cell Cycle

Mitogens and their receptors play a crucial role in controlling the progression of the cell cycle. However, the loss of mitogenic control over cell division leads to tumor formation. Therefore, mitogens and mitogen receptors play an important role in cancer research. For instance, the epidermal growth factor (EGF) - a type of mitogen and its transmembrane receptor (EGFR), decides the fate of the cell's proliferation. When EGF binds to EGFR, a member of the ErbB family of tyrosine kinase...
8.4K
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...
6.4K
mTOR Signaling and Cancer Progression03:03

mTOR Signaling and Cancer Progression

The mammalian target of rapamycin or mTOR protein was discovered in 1994 due to its direct interaction with rapamycin. The protein gets its name from a yeast homolog called TOR. The mTOR protein complex in mammalian cells plays a major role in balancing anabolic processes such as the synthesis of proteins, lipids, and nucleotides and catabolic processes, such as autophagy in response to environmental cues, such as availability of nutrients and growth factors.
The mTOR pathway or the...
5.1K
Interactions Between Signaling Pathways01:19

Interactions Between Signaling Pathways

Signaling cascades usually lack linearity. Multiple pathways interact and regulate one another, allowing cells to integrate and respond to diverse environmental stimuli.
Convergence and divergence, and cross-talk between signaling pathways
Two distinct signaling pathways can converge on a single functional unit, which may either be a single protein or a complex of proteins. The response is either functionally distinct or synergistic between the two pathways but different from the response...
7.9K
MAPK Signaling Cascades01:07

MAPK Signaling Cascades

Mitogen-activated protein kinase, or MAPK pathway, activates three sequential kinases to regulate cellular responses such as proliferation, differentiation, survival, and apoptosis. The canonical MAPK pathway starts with a mitogen or growth factor binding to an RTK. The activated RTKs stimulate Ras, which recruits Raf or MAP3 Kinase (MAPKKK), the first kinase of the MAPK signaling cascade. Raf further phosphorylates and activates MEK or MAP2 Kinases (MAPKK), which in turn phosphorylates MAP...
9.3K