β1 And β3 integrins have different roles in the adhesion and migration of vascular smooth muscle cells on extracellular matrix

Clyman, Ronald I.; Mauray, Françoise; Kramer, Randall H.

doi:10.1016/0014-4827(92)90173-6

Cited by 176 publications

(95 citation statements)

References 46 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Previous studies have shown that the αvβ3 and αvβ5 integrins mediate VSMC migration on vitronectin (Clyman et al, 1992;Kappert et al, 2001;Stawowy et al, 2004). In this regard, we investigated the effects of function-blocking antibodies against αvβ3 and αvβ5 integrins on the adhesion of aortic VSMCs to βig-h3.…”

Section: Resultsmentioning

confidence: 96%

“…For example, vitronectin has been shown to mediate VSMC adhesion mainly through the αvβ5 integrin but not through the αvβ3 integrin (Clyman et al, 1992;Kappert et al, 2001;Stawowy et al, 2004). Both the αvβ3 and αvβ5 integrins are elevated during neointima formation in injured aorta (Kappert et al, 2001).…”

Section: Discussionmentioning

confidence: 99%

“…Different integrins mediate binding of different cell types to specific matrix proteins such as collagen (e.g., α1β1, α2β1) or fibronectin (e.g., αvβ3, α5β1) (Hynes, 2002). Among them, β1 and β3 integrins have been involved in the adhesion and migration of VSMCs on fibronectin, laminin, and collagen (Clyman et al, 1990;Clyman et al, 1992). In addition to adhesion, integrins initiate intracellular signaling pathways by recruiting and activating protein kinases such as focal adhesion kinase (FAK).…”

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

βig-h3 triggers signaling pathways mediating adhesion and migration of vascular smooth muscle cells through αvβ5 integrin

Lee

Bae²,

Park³

et al. 2006

Exp Mol Med

View full text Add to dashboard Cite

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 signalregulated 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.

show abstract

Section: Resultsmentioning

confidence: 96%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

βig-h3 triggers signaling pathways mediating adhesion and migration of vascular smooth muscle cells through αvβ5 integrin

Lee

Bae²,

Park³

et al. 2006

Exp Mol Med

View full text Add to dashboard Cite

show abstract

“…7A, where the fit for active PAI-1 yields a range of 100% and clearly goes to zero, while the range obtained with PAI-1 R is only 85% and instead of going to zero approaches an asymptotic value of ϳ85% inhibition of angiogenesis. This suggests that, as in vitro (52), vitronectin in the matrix may enhance vascular cell migration and possibly vessel formation. In this case, it may be that the inhibition of angiogenesis by PAI-1 R results from the capacity of this noninhibitory mutant to block vitronectin's enhancement of vascular cell migration and/or vessel formation in vivo.…”

Section: Fig 7 Inhibition Of Angiogenesis By Noninhibitory Pai-1 R mentioning

confidence: 92%

Inhibition of Angiogenesis in Vivo by Plasminogen Activator Inhibitor-1

Stefansson

Petitclerc

Wong

et al. 2001

Journal of Biological Chemistry

157

147

View full text Add to dashboard Cite

The process of angiogenesis is important in both normal and pathologic physiology. However, the mechanisms whereby factors such as basic fibroblast growth factor promote the formation of new blood vessels are not known. In the present study, we demonstrate that exogenously added plasminogen activator inhibitor-1 (PAI-1) at therapeutic concentrations is a potent inhibitor of basic fibroblast growth factor-induced angiogenesis in the chicken chorioallantoic membrane. By using specific PAI-1 mutants with either their vitronectin binding or proteinase inhibitor activities ablated, we show that the inhibition of angiogenesis appears to occur via two distinct but apparently overlapping pathways. The first is dependent on PAI-1 inhibition of proteinase activity, most likely chicken plasmin, while the second is independent of PAI-1's anti-proteinase activity and instead appears to act through PAI-1 binding to vitronectin. Together, these data suggest that PAI-1 may be an important factor regulating angiogenesis in vivo.

show abstract

“…Integrins constitute a large family of cell membrane receptors for extracellular matrix proteins and regulate cell adhesion and migration (Clyman et al, 1992;Preissner and Sei ert, 1998;Byzova et al, 1998;Slepian et al, 1998). VN is a substrate (ligand) for four integrin receptors, a v b 1 , a v b 3 , a v b 5 and a IIb b 3 .…”

Section: Introductionmentioning

confidence: 99%

Urokinase/urokinase receptor and vitronectin/αvβ3 integrin induce chemotaxis and cytoskeleton reorganization through different signaling pathways

et al. 2001

View full text Add to dashboard Cite

Vitronectin (VN) and pro-urokinase (pro-uPA) stimulated migration of rat smooth muscle cells in a dosedependent and additive way, and induced motile-type changes in cell morphology together with a complete reorganization of the actin ®laments and of the microtubules. All these e ects were inhibited by pertussis toxin, or by antibodies directed against the urokinase receptor (uPAR) or against the VN receptor a v b 3 suggesting that an association between the two receptors is required to mediate both signals. Investigation of the signaling pathways showed that increasing the intracellular cAMP resulted in a selective inhibition of VNinduced cell migration. On the other hand, PD 98059, an inhibitor of MEK, di erentially inhibited the pro-uPAbut not the VN-induced cell migration. Phosphorylation and nuclear translocation of Erk by pro-uPA was directly observed. We conclude that the signaling pathways of pro-uPA and VN must be at least in part di erent. Oncogene (2001Oncogene ( ) 20, 2032Oncogene ( ± 2043

show abstract

β1 And β3 integrins have different roles in the adhesion and migration of vascular smooth muscle cells on extracellular matrix

Cited by 176 publications

References 46 publications

βig-h3 triggers signaling pathways mediating adhesion and migration of vascular smooth muscle cells through αvβ5 integrin

βig-h3 triggers signaling pathways mediating adhesion and migration of vascular smooth muscle cells through αvβ5 integrin

Inhibition of Angiogenesis in Vivo by Plasminogen Activator Inhibitor-1

Urokinase/urokinase receptor and vitronectin/αvβ3 integrin induce chemotaxis and cytoskeleton reorganization through different signaling pathways

Contact Info

Product

Resources

About