Time course of smooth muscle cell proliferation in the intima and media of arteries following experimental angioplasty.

Hanke, Hartmut; Strohschneider, T.; Oberhoff, Martin; Betz, E.; Karsch, Karl R.

doi:10.1161/01.res.67.3.651

Cited by 276 publications

(103 citation statements)

References 40 publications

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“…1,2 Proliferation of vascular smooth muscle cells (VSMCs) plays a pivotal role in restenosis after vessel injury associated with coronary intervention. 3,4 Consistent with this observation, inhibition of VSMC proliferation decreases neointimal cellularity after balloon injury. 5 In contrast to the role of VSMCs in restenosis, migration of VSMCs into the neointima is a determinant of plaque vulnerability.…”

supporting

confidence: 70%

Augmentation of Proliferation of Vascular Smooth Muscle Cells by Plasminogen Activator Inhibitor Type 1

Chen

Budd

Kelm

et al. 2006

ATVB

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Objective-Proliferation of vascular smooth muscle cells (VSMCs) contributes to restenosis after coronary intervention.We have shown previously that increased expression of plasminogen activator inhibitor type 1 (PAI-1) limits VSMC apoptosis. Because apoptosis and proliferation appear to be linked, we sought to determine whether increased PAI-1 would affect VSMC proliferation. Methods and Results-VSMCs were explanted from control and transgenic mice (SM22-PAI ϩ ) in which VSMC expression of PAI-1 was increased. Increased growth of SM22-PAI ϩ -VSMCs (2.3Ϯ0.4-fold) reflected, at least partially, increased proliferation. Greater expression of FLICE-like inhibitory protein (FLIP; 2.7-fold) and its cleaved active form were seen in SM22-PAI ϩ -VSMCs. The balance between caspase-8 and FLIP favored proliferation in SM22-PAI ϩ -VSMCs. Increased expression of NF-B and activation of extracellular signal-regulated kinase (ERK) were demonstrated in SM22-PAI ϩ -VSMCs (foldϭNF-Bϭ2.2Ϯ0.1, foldϭphosphorylated-ERKϭ1.6Ϯ0.1). Results were confirmed when expression of PAI-1 was increased by transfection. Inhibition of NF-B and ERK attenuated proliferation in SM22-PAI ϩ -VSMCs. Increased expression of PAI-1 promoted proliferation when VSMCs were exposed to tumor necrosis factor (TNF). Conclusions-Increased expression of PAI-1 is associated with greater activity of FLIP that promotes VSMC proliferation through NF-B and ERK. Thus, when vascular wall expression of PAI-1 is increased, restenosis after coronary intervention is likely to be potentiated by greater proliferation of VSMC and resistance to apoptosis.

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supporting

confidence: 70%

Augmentation of Proliferation of Vascular Smooth Muscle Cells by Plasminogen Activator Inhibitor Type 1

Chen

Budd

Kelm

et al. 2006

ATVB

View full text Add to dashboard Cite

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“…Thus, the timing of SMC growth in our experimental conditions is very similar to that found in the intimal thickening induced by balloon catheter injury in the rabbit aorta 31 -34 and in the rat carotid artery, 35 -37 as well as in the atherosclerotic carotid artery of rabbits after angioplasty. 28 The fact that the migration of medial SMCs into the intima continues even after the LI in the media reaches the baseline level is in agreement with the possibility of migration of nondrviding medial SMCs into the intima. 33 This is consistent with the finding that not all intimal SMCs are able to incorporate BrdU.…”

Section: Discussionsupporting

confidence: 74%

Aortic intimal thickening and myosin isoform expression in hyperthyroid rabbits.

Giuriato

Borrione

Zanellato

et al. 1991

Arterioscler Thromb

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“…During early stages of vascular lesion formation, the expression of the fully spliced Id3 protein is increased when the proliferative index of the neointima is high, suggesting that Id3 acts to promote SMC growth in response to vascular injury (26,27). Consistent with this hypothesis, ectopic Id3 expression promoted SMC proliferation and S-phase entry, whereas Id3 Ϫ/Ϫ SMC displayed reduced proliferation and S-phase entry.…”

Section: Discussionmentioning

confidence: 66%

Intron Retention Generates a Novel Id3 Isoform That Inhibits Vascular Lesion Formation

Forrest

Barringhaus

Perlegas

et al. 2004

Journal of Biological Chemistry

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The expression of intron-containing messages has been shown to occur in a variety of diseases including lactic acidosis, Cowden Syndrome, and several cancers. However, it is unknown whether these intron-containing messages result in protein production in vivo. Indeed, intron-containing RNAs are typically retained in the nucleus, targeted for degradation, or are repressed translationally. Here, we show that during vascular lesion formation in rats, an alternative isoform of the helix-loop-helix transcription factor Id3 (Id3a) generated by intron retention is abundantly expressed. We demonstrate that Id3 is expressed early in lesion formation when the proliferative index of the neointima is highest and that Id3 promotes smooth muscle cell (SMC) proliferation and S-phase entry and inhibits transcription of the cell-cycle inhibitor p21 Cip1 . Using an Id3a-specific antibody developed by our laboratory, we show that Id3a protein is induced during vascular lesion formation and that Id3a expression peaks late when the proliferative index is low or declining and extensive apoptosis is observed. Furthermore, Id3a fails to promote SMC growth and S-phase entry or to inhibit p21 Cip1 promoter transactivation. In contrast, Id3a stimulates SMC apoptosis and inhibits endogenous Id3 production. Adenoviral delivery of Id3a inhibited lesion formation in balloon-injured rat carotid arteries in vivo. These data describe a novel feedback loop whereby intron retention generates an Id3 isoform that acts to limit SMC growth during vascular lesion formation, providing the first evidence that regulated intron retention can modulate a pathologic process in vivo.

show abstract

Time course of smooth muscle cell proliferation in the intima and media of arteries following experimental angioplasty.

Cited by 276 publications

References 40 publications

Augmentation of Proliferation of Vascular Smooth Muscle Cells by Plasminogen Activator Inhibitor Type 1

Augmentation of Proliferation of Vascular Smooth Muscle Cells by Plasminogen Activator Inhibitor Type 1

Aortic intimal thickening and myosin isoform expression in hyperthyroid rabbits.

Intron Retention Generates a Novel Id3 Isoform That Inhibits Vascular Lesion Formation

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