Injury-inducible yin yang-1 inhibits vascular smooth muscle cell growth and intimal thickening by repressing P21WAF1/CIP1 transcription and perturbing cyclin D1-CDK4-P21WAF1/CIP1 assembly

Santiago, Fernando S.; Ishii, Hiroko; Hulett, Mark D.; Bobik, Alexander; Martin, John F.; Chesterman, Colin N.; Zachary, Ian; Khachigian, Levon M.

doi:10.1016/j.vph.2006.08.160

Cited by 10 publications

(13 citation statements)

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“…Interestingly, the repression of c-jun transcription by HDAC inhibition was also conferred through HDAC 3 30. Both the NF-κB and AP-1 transcriptional signaling pathways are activated during the mitogenic response of SMC, and CDK4/cyclin D1 activity is induced during neointima formation 33–35. Considering further that overexpression of cyclin D1 induces SMC proliferation,36 we would infer that the silencing of cyclin D1 expression by histone acetylation contributes at least in part to the inhibition of SMC proliferation by the HDAC inhibitor Scriptaid.…”

Section: Discussionmentioning

confidence: 99%

Epigenetic Regulation of Vascular Smooth Muscle Cell Proliferation and Neointima Formation by Histone Deacetylase Inhibition

Findeisen

Gizard

Zhao

et al. 2011

ATVB

118

101

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Objective-Proliferation of smooth muscle cells (SMC) in response to vascular injury is central to neointimal vascular remodeling. There is accumulating evidence that histone acetylation constitutes a major epigenetic modification for the transcriptional control of proliferative gene expression; however, the physiological role of histone acetylation for proliferative vascular disease remains elusive. Methods and Results-In the present study, we investigated the role of histone deacetylase (HDAC) inhibition in SMC proliferation and neointimal remodeling. We demonstrate that mitogens induce transcription of HDAC 1, 2, and 3 in SMC. Short interfering RNA-mediated knockdown of either HDAC 1, 2, or 3 and pharmacological inhibition of HDAC prevented mitogen-induced SMC proliferation. The mechanisms underlying this reduction of SMC proliferation by HDAC inhibition involve a growth arrest in the G 1 phase of the cell cycle that is due to an inhibition of retinoblastoma protein phosphorylation. HDAC inhibition resulted in a transcriptional and posttranscriptional regulation of the cyclin-dependent kinase inhibitors p21 Cip1 and p27 Kip. Furthermore, HDAC inhibition repressed mitogen-induced cyclin D1 mRNA expression and cyclin D1 promoter activity. As a result of this differential cell cycle-regulatory gene expression by HDAC inhibition, the retinoblastoma protein retains a transcriptional repression of its downstream target genes required for S phase entry. Finally, we provide evidence that these observations are applicable in vivo by demonstrating that HDAC inhibition decreased neointima formation and expression of cyclin D1 in a murine model of vascular injury. Conclusion-These

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Section: Discussionmentioning

confidence: 99%

Epigenetic Regulation of Vascular Smooth Muscle Cell Proliferation and Neointima Formation by Histone Deacetylase Inhibition

Findeisen

Gizard

Zhao

et al. 2011

ATVB

118

101

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show abstract

“…The left CCA was exposed at the bifurcation to the external and internal carotid artery and a 2-F embolectomy catheter (Edwards Lifesciences Corp., Irvine, California) was advanced proximally through an arteriotomy into the CCA. The catheter was inflated with 100 l of air and rotated as it was being retracted (31). The SPIO-labeled CD133 ϩ cells were labeled with 5-mol/l CellTracker Green 5-chloromethylfluorescein diacetate (Invitrogen-Molecular Probes).…”

Section: Cellsmentioning

confidence: 99%

Magnetic Tagging Increases Delivery of Circulating Progenitors in Vascular Injury

Kyrtatos

Lehtolainen

Junemann-Ramirez³

et al. 2009

JACC: Cardiovascular Interventions

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128

100

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“…One probable candidate for Nih1 is Yy1, a ubiquitous and zincfinger transcription factor. Expression of this gene results in inhibition of neointima growth in human, rabbit and rat blood vessels 24. We found that Yy1 expression levels in uninjured arterial walls were higher in C3H than in B6 by real-time PCR and immunohistochemistry.…”

Section: Discussionmentioning

confidence: 70%

Quantitative Trait Locus Analysis of Neointimal Formation in an Intercross Between C57BL/6 and C3H/HeJ Apolipoprotein E–Deficient Mice

Yuan

Pei

Roberts

et al. 2009

Circ Cardiovasc Genet

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Background-Inbred mouse strains C57BL/6J (B6) and C3H/HeJ (C3H) exhibit marked differences in neointimal formation after arterial injury when deficient in apolipoprotein E (apoE Ϫ/Ϫ ) and fed a Western diet. Quantitative trait locus analysis was performed on an intercross between B6.apoE Ϫ/Ϫ and C3H.apoE Ϫ/Ϫ mice to determine genetic factors contributing to the phenotype. Methods and Results-Female B6.apoE Ϫ/Ϫ mice were crossed with male C3H.apoE Ϫ/Ϫ mice to generate F 1 s, which were intercrossed to generate 204 male F 2 progeny. At 10 weeks of age, F 2 s underwent endothelium denudation injury to the left common carotid artery. Mice were fed a Western diet for 1 week before and 4 weeks after injury and analyzed for neointimal lesion size, plasma lipid, and membrane cofactor protein (MCP)-1 levels. One significant quantitative trait locus, named Nih1 (61 cM; LOD score, 5.02), on chromosome 12 and a suggestive locus on chromosome 13 (35 cM; LOD score, 2.67) were identified to influence lesion size. One significant quantitative trait locus on distal chromosome 1 accounted for major variations in plasma non-high-density lipoprotein cholesterol and triglyceride levels. Four suggestive quantitative trait locis on chromosomes 1, 2, and 3 were detected for circulating MCP-1 levels. No correlations were observed between neointimal lesion size and plasma lipid levels or between lesion size and plasma MCP-1 levels. Conclusions-Neointimal formation is controlled by genetic factors independent of those affecting plasma lipid levels and circulating MCP-1 levels in the B6 and C3H mouse model. (Circ Cardiovasc Genet. 2009;2:220-228.)

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Injury-inducible yin yang-1 inhibits vascular smooth muscle cell growth and intimal thickening by repressing P21WAF1/CIP1 transcription and perturbing cyclin D1-CDK4-P21WAF1/CIP1 assembly

Cited by 10 publications

References 0 publications

Epigenetic Regulation of Vascular Smooth Muscle Cell Proliferation and Neointima Formation by Histone Deacetylase Inhibition

Epigenetic Regulation of Vascular Smooth Muscle Cell Proliferation and Neointima Formation by Histone Deacetylase Inhibition

Magnetic Tagging Increases Delivery of Circulating Progenitors in Vascular Injury

Quantitative Trait Locus Analysis of Neointimal Formation in an Intercross Between C57BL/6 and C3H/HeJ Apolipoprotein E–Deficient Mice

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