Related Experiment Video

Updated: Feb 18, 2026

Myeloid Innate Signaling Pathway Regulation by MALT1 Paracaspase Activity
07:09

Myeloid Innate Signaling Pathway Regulation by MALT1 Paracaspase Activity

Published on: January 7, 2019

8.0K

DUSP19 regulates IL-1β-induced apoptosis and MMPs expression in rat chondrocytes through JAK2/STAT3 signaling pathway

Zi-Zhou Yao1, Ai-Xin Hu1, Xiang-Sheng Liu2

  • 1The Department of Orthopedic Surgery, People's Hospital of Three Gorges University, Yichang, Hubei Province, China.

Biomedicine & Pharmacotherapy = Biomedecine & Pharmacotherapie
|November 28, 2017
PubMed

Insights

Dual specificity phosphatase 19 (DUSP19) protects chondrocytes from apoptosis in osteoarthritis by inhibiting the JAK2/STAT3 pathway. Upregulating DUSP19 reduces inflammation-induced cell death and matrix metalloproteinase expression.

Area of Science:

  • Biochemistry
  • Cell Biology
  • Molecular Biology

Background:

  • Osteoarthritis (OA) is characterized by articular cartilage degeneration and chondrocyte apoptosis.
  • The JAK2/STAT3 signaling pathway plays a role in OA pathogenesis.

Purpose of the Study:

  • To investigate the role of DUSP19 in IL-1β-induced chondrocyte apoptosis.
  • To determine if DUSP19 influences the JAK2/STAT3 pathway in rat chondrocytes.

Main Methods:

  • Chondrocytes were treated with IL-1β, DUSP19-expressing constructs, DUSP19-RNA interference, and/or AG490 (JAK2/STAT3 inhibitor).
  • Gene and protein expression (DUSP19, apoptosis markers, JAK2/STAT3, p-JAK2, p-STAT3) were analyzed using Real-time PCR and Western blot.
  • Cell viability and apoptosis were assessed using CCK-8 assay and Annexin V/propidium iodide staining.

Main Results:

  • IL-1β decreased DUSP19 expression and chondrocyte viability in a dose-dependent manner.
  • DUSP19 upregulation inhibited IL-1β-induced JAK2/STAT3 activation and chondrocyte apoptosis.
  • DUSP19 downregulation mimicked IL-1β effects, while AG490 inhibited JAK2/STAT3 activation and apoptosis.

Conclusions:

  • DUSP19 upregulation inhibits IL-1β-induced chondrocyte apoptosis and matrix metalloproteinase (MMP) expression.
  • This protective effect is mediated by the inactivation of the JAK2/STAT3 pathway.
Keywords:
ApoptosisChondrocyteDUSP19JAK2Matrix metalloproteinasesOsteoarthritisSTAT3

More Related Videos

Mechanism of Kemeng Fang's Inhibition of Podocyte Apoptosis in Rats with Membranous Nephropathy through the PI3K/AKT Signaling Pathway07:15

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

967

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...
13.2K
NF-κB-dependent Signaling Pathway02:26

NF-κB-dependent Signaling Pathway

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...
10.1K
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...
10.6K
Caspases01:24

Caspases

Caspase, a family of cysteine proteases, serve as effectors in apoptosis. The ced3 gene in C.elegans was first identified to be involved in apoptosis. This gene encodes the ced-3 caspase that is similar to the interleukin-1-beta converting enzyme or ICE in mammals. In addition to apoptosis, caspases also function in the inflammatory response. Inflammatory caspases are essential in activating pro-inflammatory cytokines that recruit immune cells and block the replication of pathogens inside...
14.3K
Role of Matrix Metalloproteases in Degradation of ECM01:23

Role of Matrix Metalloproteases in Degradation of ECM

Matrix metalloproteases (MMPs) are enzymes involved in the hydrolysis of proteins and glycoproteins of the extracellular matrix. MMPs are essential for the migration and proliferation of cells through the dense matrix network, throughout embryonic development, and throughout morphogenesis. The first MMP activity discovered was a collagenase in a tadpole's tail undergoing metamorphosis. The active collagen deposition and modifications lead to the morphogenesis of tadpoles into the adult...
3.5K
The Extrinsic Apoptotic Pathway01:17

The Extrinsic Apoptotic Pathway

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...
8.8K