Related Experiment Video

Updated: Aug 20, 2026

Mechanism of Regulation of Adipocyte Numbers in Adult Organisms Through Differentiation and Apoptosis Homeostasis
08:34

Mechanism of Regulation of Adipocyte Numbers in Adult Organisms Through Differentiation and Apoptosis Homeostasis

Published on: June 3, 2016

Negative regulation of adipogenesis from human mesenchymal stem cells by Jun N-terminal kinase

Sachiko Tominaga1, Tomohiro Yamaguchi, Shin-Ichiro Takahashi

  • 1Graduate School of Life Science, Himeji Institute of Technology, University of Hyogo, 3-2-1 Koto, Kamigori, Hyogo 678-1297, Japan.

Biochemical and Biophysical Research Communications
|December 8, 2004
PubMed

Insights

Jun N-terminal kinase (JNK) inhibition using SP600125 promotes human mesenchymal stem cell (hMSC) adipogenesis while repressing osteogenesis. JNK signaling negatively regulates adipogenesis by affecting transcription factors and CRE-binding protein activity.

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Stem Cell Research

Background:

  • Human mesenchymal stem cells (hMSCs) exhibit multipotency, differentiating into adipocytes, osteoblasts, and chondrocytes.
  • The precise molecular mechanisms regulating hMSC differentiation pathways remain under investigation.

Purpose of the Study:

  • To investigate the role of Jun N-terminal kinase (JNK) signaling in regulating adipogenesis and osteogenesis in hMSCs.
  • To elucidate the molecular targets of JNK inhibition in the context of stem cell differentiation.

Main Methods:

  • Treatment of hMSCs with SP600125, a specific JNK inhibitor.
  • Analysis of adipogenic and osteogenic gene expression.
  • Gene reporter assays to assess transcriptional activity.

Main Results:

  • SP600125 treatment promoted adipogenesis and repressed osteogenesis in hMSCs.
  • JNK inhibition upregulated key adipogenic transcription factors (C/EBPα, C/EBPβ, PPARγ2).
  • SP600125 and dominant-negative JNK enhanced cAMP-response element (CRE) transcriptional activity, indicating JNK's repressive role.

Conclusions:

  • JNK signaling plays a critical role in repressing adipogenesis in hMSCs.
  • JNK likely inhibits adipogenesis by suppressing the transactivating function of CRE-binding protein.
  • JNK-mediated phosphorylation of insulin receptor substrate-1 may also contribute to adipogenesis repression.

More Related Videos

Robust Differentiation of Human iPSCs into a Pure Population of Adipocytes to Study Adipocyte-Associated Disorders10:31

Robust Differentiation of Human iPSCs into a Pure Population of Adipocytes to Study Adipocyte-Associated Disorders

Published on: February 9, 2022

Semi-Automated Isolation of the Stromal Vascular Fraction from Murine White Adipose Tissue Using a Tissue Dissociator06:08

Semi-Automated Isolation of the Stromal Vascular Fraction from Murine White Adipose Tissue Using a Tissue Dissociator

Published on: May 19, 2023

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...
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...
Mesenchymal Stem Cells01:19

Mesenchymal Stem Cells

Mesenchymal stem cells (MSCs) are adult stem cells that can differentiate into most connective tissue cell types, except for hematopoietic cells, depending upon the source of MSCs. For example, bone-marrow-derived MSCs (BM-MSCs) can differentiate into osteocytes, hepatocytes, and pancreatic and neuronal cells. MSCs can be isolated from various sources such as bone marrow, placenta, adipose tissue, teeth, and Wharton’s jelly, a gelatinous substance in the umbilical cord. The ease of their access...
Master Transcription Regulators02:23

Master Transcription Regulators

Master transcription regulators are regulatory proteins that are predominantly responsible for regulating the expression of multiple genes. Often these genes work in concert to drive a  complex process. Activation of a master transcription regulator can lead to a cascade of transcriptional activation necessary for that outcome. These regulators can directly bind to the regulatory sequences of the various genes involved, or they can indirectly regulate transcription by binding to regulatory...
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...