α8β1 Integrin is up-regulated in the neointima concomitant with late luminal loss after balloon injury

Zargham, Ramin; Pepin, Julie; Thibault, Gaétan

doi:10.1016/j.carpath.2007.01.010

Cited by 18 publications

(16 citation statements)

References 31 publications

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“…We have shown previously [53] that, at 7 days after balloon injury in the rat carotid artery, there is a down-regulation of α8β1 integrin concomitant with the loss of contractile phenotype in the tunica media. On the other hand, we have reported recently [54] the up-regulation of SM α-actin and α8β1 integrin as contractile markers in the neointima at 21 days after balloon injury of rat carotid arteries (Figure 1). This up-regulation was concomitant with late lumen loss.…”

Section: Mechanism Of Constrictive Remodellingmentioning

confidence: 93%

“…This up-regulation was concomitant with late lumen loss. Moreover, α8β1 integrin and SM α-actin were localized at the medial side of the neointima where there was an intense expression of collagen and fibronectin, two hallmarks of active constrictive remodelling [54]. At 28 days, when there was evidence of arterial shrinkage (reduced size of the neointima as well as arterial circumference), α8 integrin became more upregulated and spread throughout the complete neointima.…”

Section: Mechanism Of Constrictive Remodellingmentioning

confidence: 97%

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Preventing restenosis after angioplasty: a multistage approach

Zargham

2008

Clinical Science

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Arterial reconstruction procedures, including balloon angioplasty, stenting and coronary artery bypass, are used to restore blood flow in atherosclerotic arteries. Restenosis of these arteries has remained a major limitation of the application of these procedures, especially in the case of balloon angioplasty. Post-angioplasty restenosis results from two major processes: neointimal formation and constrictive remodelling. Neointimal formation is initiated by arterial injury with a resultant loss of contractile phenotype in tunica media, leading to VSMC [vascular SM (smooth muscle) cell] migration from the tunica media to the intima. Migrated VSMCs contribute to the intimal thickening by the excessive synthesis of ECM (extracellular matrix) and proliferation. However, increased neointimal mass is not solely responsible for luminal narrowing. Inward constrictive remodelling is also considered as a major cause of delayed failure of angioplasty. At later stages after angioplasty, the increase in contractile forces leads to lumen narrowing. Recent studies show that SM contractile proteins are re-expressed in the neointima, concomitant with late lumen loss. Therefore one important question is whether the restoration of contractile phenotype, which can suppress VSMC migration, is favourable or detrimental. In this review, the importance of viewing restenosis as a multistage process is discussed. Different stages of restenosis occur in a sequential manner and are related to each other, but in each stage a different strategy should be taken into consideration to reduce restenosis. Defining the role of each process not only reshapes the current concept, but also helps us to target restenosis with more efficacy.

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Section: Mechanism Of Constrictive Remodellingmentioning

confidence: 93%

Section: Mechanism Of Constrictive Remodellingmentioning

confidence: 97%

Preventing restenosis after angioplasty: a multistage approach

Zargham

2008

Clinical Science

Self Cite

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“…24 Moreover, TGFb-induced myofibroblastic features are impaired in a8 knocked down fibroblasts. 47 On the other hand, in VSMCs that exhibit a less contractile phenotype, high-passage cells, a8 integrin overexpression elicits the restoration of contractile phenotype characteristics. 16 Therefore, a8 integrin seems to exert a prominent role on both sides of VSMC phenotypic transition.…”

Section: A8 Integrin and Contractile Ability In Vsmcmentioning

confidence: 99%

“…47 It seems likely that a8 integrin downregulation can shut down the mechanisms responsible for the VSMC contractile phenotype. It is well-documented that RhoA activity is critical for controlling the VSMC contractile phenotype, 48 the assembly of actin stress fibers and focal adhesions.…”

Section: A8 Integrin and Contractile Ability In Vsmcmentioning

confidence: 99%

“…59 The role of tension in the morphogenesis and function of these cells has also been reported. 60 When we look at the pathological conditions in which a8 expression is increased, for example, after injury in models of pulmonary and hepatic fibrosis, in carotid constrictive remodeling after angioplasty or glomerulonephritis 13,47,61 there is one property in common. In these fibrotic organs, tensile forces are increased.…”

Section: Tension-dependent Growth and A8 Integrinmentioning

confidence: 99%

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