Expression of coxsackievirus and adenovirus receptor in neointima of the rat carotid artery

Nasuno, Akimitsu; Toba, Kenji; Ozawa, Tomohiro; Hanawa, Haruo; Osman, Yasser; Hotta, Yuko; Yoshida, Kaori; Sawada, Takashi; Kato, Kiminori; Kuwano, Ryozo; Watanabe, Kenichi; Aizawa, Yoshifusa

doi:10.1016/s1054-8807(03)00137-6

Cited by 12 publications

(12 citation statements)

References 24 publications

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“…Adenovirus-based gene therapy can be a potential treatment mode for different human disease; neurodegenerative diseases such as Parkinson´s and Alzheimer´s disease, vascular diseases and retinal diseases [21][22][23]. Today, focus has mostly been on therapy of tumours of different origin [24].…”

Section: Discussionmentioning

confidence: 99%

Cell type- and region- dependent coxsackie adenovirus receptor expression in the central nervous system

et al. 2005

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Section: Discussionmentioning

confidence: 99%

Cell type- and region- dependent coxsackie adenovirus receptor expression in the central nervous system

et al. 2005

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“…The availability of CAR on cell surface is a determining factor of a cell's susceptibility to adenoviral vectors for gene delivery [2]. Therefore, extensive studies have been carried out to establish the expression profile of CAR in a variety of human tissues that are of interest to gene therapy, such as brain, heart and muscles [3][4][5][6].…”

Section: Introductionmentioning

confidence: 99%

Coxsackie and adenovirus receptor (CAR) is a product of Sertoli and germ cells in rat testes which is localized at the Sertoli–Sertoli and Sertoli–germ cell interface

Wang

Mruk

Lee

et al. 2007

Experimental Cell Research

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The coxsackie and adenovirus receptor (CAR), a putative cell-cell adhesion molecule, has attracted wide interest due to its importance in viral pathogenesis and in mediating adenoviral gene delivery. However, the distribution pattern and physiological function of CAR in the testis is still not clear. Here, we identified CAR in Sertoli cells and germ cells of rats. In vivo studies have shown that CAR resides at the blood-testis barrier as well as at the ectoplasmic specialization. The persistent expression of CAR in rat testes from neonatal period throughout adulthood implicates its role in spermatogenesis. Using primary Sertoli cell cultures, we observed a significant induction of CAR during the formation of Sertoli cell epithelium. Furthermore, CAR was seen to be concentrated at inter-Sertoli cell junctions, colocalizing with tight junction protein marker ZO-1 and adherens junction protein N-cadherin. CAR was also found to be associated with proteins of Src kinase family and its protein level declined after TNFα treatment in Sertoli cell cultures. Immunofluorescent staining of isolated germ cells has revealed the presence of CAR on spermatogonia, spermatocytes, round spermatids and elongate spermatids. Taken together, we propose that CAR functions as an adhesion molecule in maintaining the inter-Sertoli cell junctions at the basal compartment of the seminiferous epithelium. In addition, CAR may confer adhesion between Sertoli and germ cells at the Sertoli-germ cell interface. It is possible that the receptor utilized by viral pathogens to breakthrough the epithelial barrier was also employed by developing germ cells to migrate through the inter-Sertoli cell junctions.

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“…PCNA is expressed in growing cells. CAR together with PCNA was abundantly expressed in the neointima of the rat carotid artery, and declined to a basal level after the regeneration of EC (Nasuno et al 2004). In the present study, the growing SMCs in the cul-ture highly expressed CAR from days 1 to 3.…”

Section: Cultured Smcmentioning

confidence: 94%

“…Culture slides were harvested, washed with PBS, fixed with ice-cold Zamboni solution for 30 min, and stained for CAR and proliferating cell nuclear antigen (PCNA). CAR was stained by serial incubation with rabbit anti-CAR (Nasuno et al 2004), biotinylated goat anti-rabbit Ig (Nichirei, Tokyo, Japan) and FITC-conjugated streptavidin (Vector, Burlingame, CA). PCNA was stained using mouse anti-PCNA (Zymed, San Francisco, CA) and TRITC-conjugated goat anti-mouse IgG (Vector).…”

Section: Culture Of Vascular Smcsmentioning

confidence: 99%

“…CAR is one of the adhesion molecules of the Ig-superfamily, and its extracellular domain is homologous to the vascular cell adhesion molecule (VCAM) and the intercellular adhesion molecule (ICAM) (Bergelson et al 1997). CAR is a homophilic receptor/ligand , and may function as a sensor of cell-cell interaction to control the healing process of vascular injury (Nasuno et al 2004).…”

Section: Balloon Injury Modelmentioning

confidence: 99%

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Imatinib Mesilate Inhibits Neointimal Hyperplasia via Growth Inhibition of Vascular Smooth Muscle Cells in a Rat Model of Balloon Injury

Makiyama

Toba

Kato

et al. 2008

Tohoku J. Exp. Med.

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Restenosis is a major problem in percutaneous catheter intervension (PCI) for coronary artery stenosis in patients with acute myocardial infarction. Coronary restenosis arises from intimal hyperplasia, i.e., hyperplasia of the vascular smooth muscle cells (SMCs) caused by endothelial cell (EC) damage due to PCI. Drug eluting stent (DES), a novel stent coated with a cell-growth inhibitor, such as rapamycin, has been utilized to block SMC proliferation, but DES also blocks EC repair and thus requires the administration of anti-platelets for a long time to prevent thrombus formation after PCI. Moreover, insufficient prevention of platelet aggregation sometimes induces restenosis after PCI. One of the signal transduction inhibitors, imatinib mesilate, blocks tyrosine kinase activity of platelet-derived growth factor receptor (PDGFR), and therefore it may block the development of neointima through growth inhibition of SMCs without the obstructive effect on EC-repair. We therefore studied the effects of imatinib on neointimal hyperplasia in a balloon injury model of rat carotid arteries. Rats were orally administered with imatinib for 14 days after balloon injury, and sacrificed to analyze the neointimal formation. Intimal hyperplasia was inhibited by imatinib in a dose-dependent manner. Therefore imatinib presumably obstructed the growth of SMCs via interception on growth-signaling of PDG-FR. The administration of imatinib after coronary stenting or the use of an imatinibeluting stent may further reduce the risk of restenosis in patients.coronary intervention; intimal hyperplasia; restenosis; imatinib mesilate; coxsackievirus and adenovirus receptor.Tohoku

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Expression of coxsackievirus and adenovirus receptor in neointima of the rat carotid artery

Cited by 12 publications

References 24 publications

Cell type- and region- dependent coxsackie adenovirus receptor expression in the central nervous system

Cell type- and region- dependent coxsackie adenovirus receptor expression in the central nervous system

Coxsackie and adenovirus receptor (CAR) is a product of Sertoli and germ cells in rat testes which is localized at the Sertoli–Sertoli and Sertoli–germ cell interface

Imatinib Mesilate Inhibits Neointimal Hyperplasia via Growth Inhibition of Vascular Smooth Muscle Cells in a Rat Model of Balloon Injury

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