Related Experiment Video

Updated: May 16, 2026

Chondrogenic Differentiation Induction of Adipose-derived Stem Cells by Centrifugal Gravity
08:30

Chondrogenic Differentiation Induction of Adipose-derived Stem Cells by Centrifugal Gravity

Published on: February 24, 2017

Double-stranded RNA-dependent protein kinase regulates insulin-stimulated chondrogenesis in mouse clonal chondrogenic

Hiroyuki Morimoto1, Ryoko Baba, Tatsuji Haneji

  • 1Department of Anatomy, School of Medicine, University of Occupational and Environmental Health, Iseigaoka, Yahatanishi, Kitakyushu, Fukuoka, Japan. morimoto@med.uoeh-u.ac.jp

Cell and Tissue Research
|November 27, 2012
PubMed

Insights

Double-stranded RNA-dependent protein kinase (PKR) is essential for chondrocyte differentiation, regulating cartilage matrix formation and key gene expression. Its inhibition impairs chondrogenesis, highlighting its role in skeletal development.

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Developmental Biology

Background:

  • Double-stranded RNA-dependent protein kinase (PKR) is an interferon-induced translational inhibitor involved in cell growth and differentiation.
  • Previous studies show PKR influences osteoblast and osteoclast formation, but its role in chondrogenesis is less understood.

Purpose of the Study:

  • To investigate the role of PKR in chondrogenesis using the ATDC-5 cell line.
  • To elucidate the molecular mechanisms by which PKR affects chondrocyte differentiation.

Main Methods:

  • In vitro differentiation of ATDC-5 cells with insulin.
  • Treatment with a PKR inhibitor (2-aminopurine).
  • Analysis of cartilage matrix formation (Alcian blue staining) and protein expression (STAT1, Sox-9).
  • Immunohistochemical analysis of PKR in mouse embryonic mandibular condyle cartilage.

Main Results:

  • PKR is required for in vitro chondrogenesis of ATDC-5 cells, evidenced by reduced cartilage matrix formation upon PKR inhibition.
  • PKR inhibition altered the expression patterns of STAT1 and Sox-9, crucial factors in chondrocyte differentiation.
  • PKR was detected in the mandibular condyle cartilage of mouse embryos, suggesting in vivo relevance.

Conclusions:

  • PKR plays a critical role in chondrocyte differentiation.
  • PKR modulates chondrogenesis through the regulation of STAT1 and Sox-9 expression.
  • These findings suggest PKR as a potential target for skeletal development research.

More Related Videos

Isolation of Whole Cell Protein Lysates from Mouse Facial Processes and Cultured Palatal Mesenchyme Cells for Phosphoprotein Analysis07:26

Isolation of Whole Cell Protein Lysates from Mouse Facial Processes and Cultured Palatal Mesenchyme Cells for Phosphoprotein Analysis

Published on: April 1, 2022

Related Concept Videos

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 rapamycin-insensitive companion...
DNA Damage can Stall the Cell Cycle02:36

DNA Damage can Stall the Cell Cycle

In response to DNA damage, cells can pause the cell cycle to assess and repair the breaks. However, the cell must check the DNA at certain critical stages during the cell cycle. If the cell cycle pauses before DNA replication, the cells will contain twice the amount of DNA. On the other hand, if cells arrest after DNA replication but before mitosis, they will contain four times the normal amount of DNA. With a host of specialized proteins at their disposal,cells must use the right protein at...
DNA Damage Can Stall the Cell Cycle02:36

DNA Damage Can Stall the Cell Cycle

In response to DNA damage, cells can pause the cell cycle to assess and repair the breaks. However, the cell must check the DNA at certain critical stages during the cell cycle. If the cell cycle pauses before DNA replication, the cells will contain twice the amount of DNA. On the other hand, if cells arrest after DNA replication but before mitosis, they will contain four times the normal amount of DNA. With a host of specialized proteins at their disposal,cells must use the right protein at...
Insulin: The Receptor and Signaling Pathways01:28

Insulin: The Receptor and Signaling Pathways

Insulin action is mediated through a receptor tyrosine kinase, akin to the IGF-1 receptor. The number of receptors per cell varies significantly, from 40 on erythrocytes to 300,000 on adipocytes and hepatocytes. The insulin receptor consists of linked α/β subunit dimers, forming a heterotetramer glycoprotein with two extracellular α subunits and two β subunits spanning the membrane. The α subunits inhibit the inherent tyrosine kinase activity of the β subunits, but this inhibition is released...
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...
TGF - β Signaling Pathway01:16

TGF - β Signaling Pathway

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 are of three kinds RI, RII, and RIII. The RI...