Dominant negative c-Jun gene transfer inhibits vascular smooth muscle cell proliferation and neointimal hyperplasia in rats

Yasumoto, Hideo; Kim, S; Zhan, Yumei; Miyazaki, Hitoshi; Hoshiga, Masaaki; Kaneda, Yasufumi; Morishita, Ryuichi; Itoh, Hiroshi

doi:10.1038/sj.gt.3301590

Cited by 39 publications

(36 citation statements)

References 25 publications

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“…2,3 As shown by gel mobility shift analysis in Figure 3, Ad.DN-c-Jun gene transfer increased AP-1 DNA-binding activity. However, the position of AP-1 band due to Ad.DN-c-Jun was upper to that of endogenous AP-1, being in good agreement with our previous papers.…”

Section: Cardiacmentioning

confidence: 75%

“…2,7 TAM67 has the DNA-binding domain of wild-type c-Jun. Recombinant replication-defective E1 and E3 adenoviral vectors expressing the TAM67 gene (Ad.DN-c-Jun) were constructed by using an adenovirus expression vector kit (Takara Biomedicals), according to the method of Miyake et al 8 cDNA encoding TAM67 was placed into a cassette cosmid vector, PaxCAwt, which possesses the CAG promoter, composed of a cytomegalovirus enhancer, chicken b-actin promoter, and rabbit a-globin poly(A) signal.…”

Section: Construction Of Recombinant Adenovirus Containing Dn-c-junmentioning

confidence: 99%

“…2 The membrane was immunoblotted with anti-c-Jun antibody (sc-44; Santa cruz), anti-b-galactosidase, anti-phosphop70S6 kinase (Promega), anti-p70S6 kinase (Promega), and anti-a-tubulin, using the enzyme-linked chemiluminescence (ECL) method as described previously. 2 RNA preparation and Northern blot analysis. All procedures were performed, as described in detail in our previous reports.…”

Section: Western Blot Analysismentioning

confidence: 99%

“…[2][3][4] The sequence of double-strand consensus oligonucleotides of AP-1, NF-kB, Sp-1, and CREB were previously described. Supershift assay was performed with rabbit polyclonal anti-c-Fos IgG (sc-253-G, 2 mg), anti-c-Jun IgG (sc-822X, 2 mg) recognizing the amino acids from 56 to 69 (transactivation domain) of wild c-Jun, or anti-c-Jun IgG (sc-44X, 2 mg) recognizing the conserved DNAbinding domain of wild c-Jun (all from Santa Cruz).…”

Section: Gel Mobility Shift Assaysmentioning

confidence: 99%

“…3 We found that blockade of c-Jun by gene transfer of DN-c-Jun inhibited vascular smooth muscle cell proliferation and migration in vivo or in vitro, thereby proposing that suppression of c-Jun is useful for treatment of vascular hyperplasia. 2,3 Furthermore, we have determined the activities of cardiac AP-1 in angiotensin II (AngII)-infused rats 4 and stroke-prone spontaneously hypertensive rats (SHRSP). 5 We have found that cardiac AP-1 activity, related to c-Jun, is activated in AngII-infused rats and SHRSP.…”

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confidence: 99%

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Dominant-negative c-Jun inhibits rat cardiac hypertrophy induced by angiotensin II and hypertension

et al. 2005

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Section: Cardiacmentioning

confidence: 75%

Section: Construction Of Recombinant Adenovirus Containing Dn-c-junmentioning

confidence: 99%

Section: Western Blot Analysismentioning

confidence: 99%

Section: Gel Mobility Shift Assaysmentioning

confidence: 99%

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confidence: 99%

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Dominant-negative c-Jun inhibits rat cardiac hypertrophy induced by angiotensin II and hypertension

et al. 2005

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Transcriptome of the inner circular smooth muscle of the developing mouse intestine: Evidence for regulation of visceral smooth muscle genes by the hedgehog target gene, cJun

Gurdziel

Vogt

Walton

et al. 2016

Developmental Dynamics

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Background Digestion is facilitated by coordinated contractions of the intestinal muscularis externa, a bilayered smooth muscle structure that is composed of inner circular (ICM) and outer longitudinal (OLM) muscles. We performed transcriptome analysis of intestinal mesenchyme tissue at E14.5, when the ICM, but not the OLM is present, to investigate the transcriptional program of the ICM. Results We identified 3967 genes enriched in E14.5 intestinal mesenchyme. The gene expression profiles were clustered and annotated to known muscle genes, identifying a muscle- enriched subcluster. Using publically available in situ data, 127 genes were verified as expressed in ICM. Examination of the promoter and regulatory regions for these co-expressed genes revealed enrichment for cJUN transcription factor binding sites and cJUN protein was enriched in ICM. cJUN ChIP-seq, performed at E14.5, revealed that cJUN regulatory regions contain characteristics of muscle enhancers. Finally, we show that cJUN is a target of Hedgehog (Hh), a signaling pathway known to be important in smooth muscle development, and identify a cJUN genomic enhancer that is responsive to Hh. Conclusions This work provides the first transcriptional catalog for the developing ICM and suggests that cJUN regulates gene expression in the ICM downstream of Hh signaling.

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Antagonist of microRNA‐21 improves balloon injury‐induced rat iliac artery remodeling by regulating proliferation and apoptosis of adventitial fibroblasts and myofibroblasts

Wang

Zhao

Liu

et al. 2012

J of Cellular Biochemistry

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Molecular pathways involved in adventitial fibroblasts (AFs) and myofibroblasts (MFs) proliferation and apoptosis contribute to vascular remodeling. MicroRNA-21 (miR-21) plays an important role in regulating cellular proliferation and apoptosis of many cell types; however, the effect of miR-21 on AFs and MFs is still unknown. In this study, we found that miR-21 was expressed in AFs and overexpressed in MFs. Inhibition of miR-21 decreased proliferation and increased apoptosis of AFs and MFs, and overexpression of miR-21 with pre-miR-21 had the reverse effect. Programmed cell death 4 (PDCD4), related to cell proliferation and apoptosis, was validated as a direct target of miR-21 by dual-luciferase reporter assay and gain and loss of function of miR-21 in AFs and MFs. PDCD4 knockdown with siRNA partly rescued the reduced proliferation with miR-21 inhibition and alleviated the increased apoptosis induced by miR-21 inhibition in AFs and MFs. Moreover, increasing PDCD4 expression by miR-21 inhibition significantly decreased JNK/c-Jun activity. In contrast, decreasing PDCD4 expression by pre-miR-21 treatment increased JNK/c-Jun activity, while the effect of miR-21 inhibition on JNK/c-Jun activity could be rescued by PDCD4 siRNA. Moreover, miR-21 inhibition could regulate proliferation and apoptosis of vascular AFs and MFs in vivo. Furthermore, miR-21 inhibition reversed vascular remodeling induced by balloon injury. In summary, our findings demonstrate that miR-21 may have a critical role in regulating proliferation and apoptosis of AFs and MFs, and PDCD4 is a functional target gene involved in the miR-21-mediated cellular effects in vascular remodeling by a miR-21/PDCD4/JNK/c-Jun pathway.

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Dominant negative c-Jun gene transfer inhibits vascular smooth muscle cell proliferation and neointimal hyperplasia in rats

Abstract: We previously reported that activator protein-1 (AP-1), containing c-

Cited by 39 publications

References 25 publications

Dominant-negative c-Jun inhibits rat cardiac hypertrophy induced by angiotensin II and hypertension

Dominant-negative c-Jun inhibits rat cardiac hypertrophy induced by angiotensin II and hypertension

Transcriptome of the inner circular smooth muscle of the developing mouse intestine: Evidence for regulation of visceral smooth muscle genes by the hedgehog target gene, cJun

Antagonist of microRNA‐21 improves balloon injury‐induced rat iliac artery remodeling by regulating proliferation and apoptosis of adventitial fibroblasts and myofibroblasts

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