Morphological changes and smooth muscle cell proliferation after experimental excimer laser treatment.

Hanke, Hartmut; Haase, Karl K.; Hanke, Sybille; Oberhoff, Martin; Hassenstein, S.; Betz, E.; Karsch, Karl R.

doi:10.1161/01.cir.83.4.1380

Cited by 45 publications

(13 citation statements)

References 38 publications

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“…Smooth muscle cell proliferation was measured 6 and 19 d after the injury as described (10). 18 h before harvesting of the arteries, the rats were given 100 mg/kg 5-bromo-2'-deoxyuridine (BrdU)' (Sigma Immunochemicals, St. Louis, MO) and 75 mg/kg 2'-deoxycytidine (Sigma Immunochemicals) into a subcutaneous neck depot.…”

Section: Methodsmentioning

confidence: 99%

Antibodies against transforming growth factor-beta 1 suppress intimal hyperplasia in a rat model.

Wolf¹,

Rasmussen²,

Ruoslahti³

1994

J. Clin. Invest.

289

155

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Section: Methodsmentioning

confidence: 99%

Antibodies against transforming growth factor-beta 1 suppress intimal hyperplasia in a rat model.

Wolf¹,

Rasmussen²,

Ruoslahti³

1994

J. Clin. Invest.

289

155

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“…After hybridization, tissues were washed with 4 x SSC, treated with 20 ,ug/ml ribonuclease A (RNase A) (Sigma) in 0.5 M NaCl/ 10 mM Tris, pH 8.0/1 mM EDTA to eliminate nonhybridized cRNA strands, and washed in 2 X SSC and 0.1 x SSC. After dehydration in 70, 95, and 100% alcohol containing ammonium acetate, autoradiography in Kodak NTB-2 emulsion (Eastman Kodak Co., Rochester, NY) was performed, developed after 7 d, and counterstained with hematoxylin and eosin.…”

Section: Methodsmentioning

confidence: 99%

“…It is widely accepted that smooth muscle cell proliferation is responsible for generation ofrestenotic lesions in vascular tissue (1)(2)(3)(4)(5). Although restenosis complicates balloon angioplasty in at least 40% of cases, identification of the events and specific factors responsible for restenosis remains elusive.…”

Section: Introductionmentioning

confidence: 99%

Expression of transforming growth factor-beta 1 is increased in human vascular restenosis lesions.

Nikol¹,

Isner²,

Pickering³

et al. 1992

J. Clin. Invest.

366

174

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Human atheromata obtained in vivo were used to test the hypothesis that transforming growth factor-(31 plays a role in the development of vascular restenosis.We analyzed 28 specimens from patients with primary atherosclerotic or restenotic lesions; 26 of these were obtained by directional atherectomy and 2 at the time of coronary bypass surgery. Seven control tissues included operatively excised segments of human internal mammary artery, myocardium, and unused portions of vein graft obtained intraoperatively. From these 35 specimens, 210 sections were examined using in situ hybridization. Measurement of silver grains/ nucleus disclosed that expression of transforming growth factor-ftl mRNA was highest in restenotic tissues (P < 0.001 vs. primary atherosclerotic tissues) and lowest in nonatherosclerotic (control) tissues. In cultures of human vascular smooth muscle cells grown from explants of internal mammary artery, expression of mRNA for transforming growth factor-ftl was significantly greater in subconfluent than in confluent smooth muscle cells (P = 0.05). Transforming growth factor type-ft III receptor was expressed in cell cultures and undetectable in the tissue specimens. Sections taken adjacent to those studied by in situ hybridization were examined by immunohistochemistry using antibodies against transforming growth factor-,6l and a-actin (as a marker for smooth muscle cells) and disclosed transforming growth factor-,Bl in smooth muscle cells present in these sections.These findings are consistent with the concept that transforming growth factor-,8l plays an important role in modulating repair of vascular injury, including restenosis, after balloon angioplasty. (J. Clin. Invest. 1992. 90:1582-1592 Key words:

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“…These include flexible wire, 1 balloon catheter, 2 air drying, 3 and laser injury. 4 Although such injuries do lead to neointimal formation in arteries by removing the endothelium, which can then be used for the study of atherosclerosis and restenosis after angioplasty, they all involve procedures that are relatively complicated and are difficult to control with respect to the extent of vascular injury. 5 In light of this situations, establishment of a simple and reproducible animal model of intimal thickening that occurs in response to endothelial injury would be very desirable to assist in gaining insight into the pathophysiology of neointimal formation after vascular injury and in screening potential therapeutic agents.…”

mentioning

confidence: 99%

Photochemically Induced Endothelial Injury in the Mouse as a Screening Model for Inhibitors of Vascular Intimal Thickening

Kikuchi

Umemura

Kondo

et al. 1998

ATVB

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Abstract-We have established a mouse model of intimal thickening and assessed its suitability for experimental studies of intimal thickening. Neointimal formation was observed after endothelial injury by photochemical reaction between transluminal green light and systemically administered rose Bengal, which represents a nonmechanical approach to vessel wall denudation. Intimal thickening began 7 days after endothelial injury, reached a maximum after 21 days, and then remained unchanged for as long as 42 days. Furthermore, as a consequence of neointimal proliferation, the luminal area gradually decreased. The cells in the neointimal layer were identified as smooth muscle cells by immunohistochemical staining with an ␣-actin-specific antibody. Extracellular matrix deposition in the neointima was markedly increased beyond 14 days after injury. Smooth muscle cell proliferation, as measured by pulse labeling of 5-bromo-2Ј-deoxyuridine, was identified initially in the media 2 days after vessel wall denudation, with the proliferative activity's shifting almost exclusively to the neointima within 7 days. Endothelial regeneration, as indicated by Evans blue staining, was complete within 21 days after injury. To assess the suitability of this model for experimental studies on intimal thickening, the effect of tranilast, an antiallergy drug with a broad spectrum of pharmacological actions on intimal thickening, was investigated. Tranilast (100 mg ⅐ kg Ϫ1 ⅐ d Ϫ1 PO) significantly (PϽ0.05) reduced smooth muscle cell proliferation in the neointima and media 7 days after injury and neointimal formation 21 days after injury in treated mice compared with vehicle-treated mice. This simple experimental mouse model is suitable for studying factors promoting or inhibiting intimal thickening after endothelial injury and for developing therapeutic strategies against intimal thickening.

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Morphological changes and smooth muscle cell proliferation after experimental excimer laser treatment.

Cited by 45 publications

References 38 publications

Antibodies against transforming growth factor-beta 1 suppress intimal hyperplasia in a rat model.

Antibodies against transforming growth factor-beta 1 suppress intimal hyperplasia in a rat model.

Expression of transforming growth factor-beta 1 is increased in human vascular restenosis lesions.

Photochemically Induced Endothelial Injury in the Mouse as a Screening Model for Inhibitors of Vascular Intimal Thickening

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