Abstract
Adhesion and migration of vascular smooth muscle cells (VSMCs) play an important role in the pathogenesis of atherosclerosis. These processes involve the interaction of VSMCs with extracellular matrix proteins. Here, we investigated integrin isoforms and signaling pathways mediating the adhesion and migration of VSMCs on βig-h3, a transforming growth factor (TGF)-β-inducible extracellular matrix protein that is elevated in atherosclerotic plaques. Adhesion assays showed that the αvβ5 integrin is a functional receptor for the adhesion of aortic VSMCs to βig-h3. An YH18 motif containing amino acids between 563 and 580 of βig-h3 was an essential motif for the adhesion and growth of VSMCs. Interaction between the YH18 motif and the αvβ5 integrin was responsible for the migration of VSMCs on βig-h3. Inhibitors of phosphatidylinositide 3-kinase, extracellular signal-regulated kinase (ERK), and Src kinase reduced the adhesion and migration of VSMCs on βig-h3. βig-h3 triggered phosphorylation and activation of AKT, ERK, focal adhesion kinase, and paxillin mediating the adhesion and migration of VSMCs. Taken together, these results suggest that βig-h3 and αvβ5 integrin play a role in the adhesion and migration of VSMCs during the pathogenesis of atherosclerosis.
| Original language | English |
|---|---|
| Pages (from-to) | 153-161 |
| Number of pages | 9 |
| Journal | Experimental and Molecular Medicine |
| Volume | 38 |
| Issue number | 2 |
| Publication status | Published - 2006 Apr 30 |
| Externally published | Yes |
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Keywords
- Atherosclerosis
- Integrin αvβ5
- Muscle, smooth, vascular
- Transforming growth factor β
- βIG-H3 protein
ASJC Scopus subject areas
- Biochemistry
- Molecular Medicine
- Molecular Biology
- Clinical Biochemistry
Cite this
βig-h3 triggers signaling pathways mediating adhesion and migration of vascular smooth muscle cells through αvβ5 integrin. / Lee, Byung Heon; Bae, Jong Sup; Park, Rang Woon; Kim, Jung Eun; Park, Jae Yong; Kim, In-San.
In: Experimental and Molecular Medicine, Vol. 38, No. 2, 30.04.2006, p. 153-161.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - βig-h3 triggers signaling pathways mediating adhesion and migration of vascular smooth muscle cells through αvβ5 integrin
AU - Lee, Byung Heon
AU - Bae, Jong Sup
AU - Park, Rang Woon
AU - Kim, Jung Eun
AU - Park, Jae Yong
AU - Kim, In-San
PY - 2006/4/30
Y1 - 2006/4/30
N2 - Adhesion and migration of vascular smooth muscle cells (VSMCs) play an important role in the pathogenesis of atherosclerosis. These processes involve the interaction of VSMCs with extracellular matrix proteins. Here, we investigated integrin isoforms and signaling pathways mediating the adhesion and migration of VSMCs on βig-h3, a transforming growth factor (TGF)-β-inducible extracellular matrix protein that is elevated in atherosclerotic plaques. Adhesion assays showed that the αvβ5 integrin is a functional receptor for the adhesion of aortic VSMCs to βig-h3. An YH18 motif containing amino acids between 563 and 580 of βig-h3 was an essential motif for the adhesion and growth of VSMCs. Interaction between the YH18 motif and the αvβ5 integrin was responsible for the migration of VSMCs on βig-h3. Inhibitors of phosphatidylinositide 3-kinase, extracellular signal-regulated kinase (ERK), and Src kinase reduced the adhesion and migration of VSMCs on βig-h3. βig-h3 triggered phosphorylation and activation of AKT, ERK, focal adhesion kinase, and paxillin mediating the adhesion and migration of VSMCs. Taken together, these results suggest that βig-h3 and αvβ5 integrin play a role in the adhesion and migration of VSMCs during the pathogenesis of atherosclerosis.
AB - Adhesion and migration of vascular smooth muscle cells (VSMCs) play an important role in the pathogenesis of atherosclerosis. These processes involve the interaction of VSMCs with extracellular matrix proteins. Here, we investigated integrin isoforms and signaling pathways mediating the adhesion and migration of VSMCs on βig-h3, a transforming growth factor (TGF)-β-inducible extracellular matrix protein that is elevated in atherosclerotic plaques. Adhesion assays showed that the αvβ5 integrin is a functional receptor for the adhesion of aortic VSMCs to βig-h3. An YH18 motif containing amino acids between 563 and 580 of βig-h3 was an essential motif for the adhesion and growth of VSMCs. Interaction between the YH18 motif and the αvβ5 integrin was responsible for the migration of VSMCs on βig-h3. Inhibitors of phosphatidylinositide 3-kinase, extracellular signal-regulated kinase (ERK), and Src kinase reduced the adhesion and migration of VSMCs on βig-h3. βig-h3 triggered phosphorylation and activation of AKT, ERK, focal adhesion kinase, and paxillin mediating the adhesion and migration of VSMCs. Taken together, these results suggest that βig-h3 and αvβ5 integrin play a role in the adhesion and migration of VSMCs during the pathogenesis of atherosclerosis.
KW - Atherosclerosis
KW - Integrin αvβ5
KW - Muscle, smooth, vascular
KW - Transforming growth factor β
KW - βIG-H3 protein
UR - http://www.scopus.com/inward/record.url?scp=33646811161&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=33646811161&partnerID=8YFLogxK
M3 - Article
C2 - 16672769
AN - SCOPUS:33646811161
VL - 38
SP - 153
EP - 161
JO - Experimental and Molecular Medicine
JF - Experimental and Molecular Medicine
SN - 1226-3613
IS - 2
ER -