Related Experiment Video
Updated: Dec 29, 2025

Induction of Adhesion-dependent Signals Using Low-intensity Ultrasound
Published on: May 8, 2012
Syndecan-3 in Inflammation and Angiogenesis.
Samantha Arokiasamy1, Michaela J M Balderstone1, Giulia De Rossi2
1Barts and the London School of Medicine and Dentistry, William Harvey Research Institute, Queen Mary University of London, London, United Kingdom.
Syndecan-3 (SDC3), a large cell surface molecule, has newly discovered roles beyond the brain. Research reveals its involvement in inflammatory diseases like rheumatoid arthritis and HIV infection.
Area of Science:
- Cell biology
- Molecular biology
- Immunology
Background:
- Syndecans are a family of cell surface molecules with varied biological functions.
- Syndecan-3 (SDC3) is the largest member, yet less understood compared to others.
- SDC3 null mice exhibit normal development with minor brain-related anatomical changes.
Purpose of the Study:
- To review emerging research on Syndecan-3 (SDC3) functions.
- To explore SDC3's roles in inflammatory diseases and related processes.
Main Methods:
- Literature review of recent studies on SDC3.
- Analysis of SDC3's involvement in neuronal and non-neuronal tissues.
- Investigation of SDC3's association with angiogenesis and HIV infection.
Main Results:
- SDC3 has identified roles in neuronal and brain tissues, influencing satiety.
- Recent findings indicate SDC3 expression extends beyond neuronal tissues.
- SDC3 is implicated in rheumatoid arthritis, angiogenesis, and HIV dendritic cell infection.
Conclusions:
- SDC3 possesses diverse biological functions beyond its known roles in the nervous system.
- Emerging evidence highlights SDC3's significance in inflammatory conditions and infectious diseases.
- Further research into SDC3's mechanisms in disease is warranted.
Related Concept Videos
Regulation of Angiogenesis and Blood Supply
Mechanism of Angiogenesis
Intracellular Signaling Affects Focal Adhesions
Some...
The JAK-STAT Signaling Pathway
Role of Matrix Metalloproteases in Degradation of ECM
Activation of Integrins
In "outside-in signaling," external factors in the extracellular space bind to exposed ligand binding sites on integrins. This causes the inactive protein to undergo a conformational change to become active. Integrins are often clustered on the cell membrane. Repetitive and regularly spaced ligand binding...

