Singlet oxygen and myocardial injury: Ultrastructural, cytochemical and electrocardiographic consequences of photoactivation of rose bengal

Vandeplassche, G; Bernier, Michèle; Thoné, Fred; Borgers, M.; Kusama, Yoshiki; Hearse, David J.

doi:10.1016/0022-2828(90)91462-g

Cited by 73 publications

(35 citation statements)

References 28 publications

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“…A wellestablished photochemical carotid injury model that causes thrombosis after oxidative injury was used to address this question. This type of injury likely plays an important role in the progression of vascular disease 21,22 ; however, as with any induced-thrombosis model, the injury required to elicit thrombosis may not replicate the conditions leading to spontaneous thrombosis. This model may be particularly advantageous because the injury occurs to the endothelial cell layer, which is followed by platelet and fibrin deposition.…”

Section: Discussionmentioning

confidence: 99%

Homozygosity for Factor V Leiden Leads to Enhanced Thrombosis and Atherosclerosis in Mice

et al. 2005

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Background— Activated protein C resistance due to factor V Leiden (FVL) is a common genetic risk factor for venous thrombosis in humans. Although the impact of FVL on the development of venous thrombosis is well established, its effect on arterial thrombosis and atherosclerosis is controversial. Methods and Results— To determine the effect of the FVL mutation on arterial thrombosis in the mouse, wild-type ( Fv +/+ ), heterozygous FVL ( Fv Q /+ ), and homozygous FVL ( Fv Q/Q ) mice underwent photochemical carotid arterial injury to induce occlusive thrombosis. Fv Q/Q mice formed occlusive thromboses 27±3 minutes (n=7) after the onset of injury, which was significantly shorter than that observed for Fv +/+ mice (56±7 minutes, n=9, P <0.01), whereas Fv Q /+ mice (41±7 minutes, n=5) were intermediate ( P =0.5, compared with Fv +/+ ). To determine the source of FVL relevant to the enhanced vascular thrombosis, bone marrow transplantation experiments were performed between Fv +/+ and Fv Q/Q mice. Fv Q/Q mice transplanted with Fv +/+ bone marrow formed occlusive thromboses at 35±5 minutes (n=7, P <0.05 compared with Fv +/+ mice), whereas Fv +/+ mice transplanted with Fv Q/Q bone marrow occluded at 59±7 minutes (n=6, P <0.001 compared with Fv Q/Q mice). To assess the effect of the FVL mutation on the development of atherosclerosis, Fv Q/Q mice were crossed with the atherosclerosis-prone apolipoprotein E (ApoE)–deficient strain ( ApoE −/− ) to generate Fv Q/Q ,ApoE −/− mice. By 52 weeks of age, Fv Q/Q ,ApoE −/− mice (n=8) had developed more aortic atherosclerosis (40±6% lesion area) compared with Fv +/+ ,ApoE −/− mice (15±3% lesion area; n=12, P <0.02). Conclusions— In conclusion, homozygosity for the FVL mutation in mice leads to enhanced arterial thrombosis and atherosclerosis. The source of the FVL leading to accelerated thrombosis appears to be circulating, non–platelet-derived plasma FVL.

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Section: Discussionmentioning

confidence: 99%

Homozygosity for Factor V Leiden Leads to Enhanced Thrombosis and Atherosclerosis in Mice

et al. 2005

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“…Photochemical injury is a relatively noninvasive method of inducing endothelial injury and thrombosis that is particularly useful for small animals such as mice. 8,19,20 In addition, the endothelial injury elicited by rose bengal is mediated by a superoxide anion, 21 a type of injury that may occur endogenously in the progression of atherosclerosis 22 and contribute to plaque disruption.…”

Section: Discussionmentioning

confidence: 99%

Hyperlipidemia Promotes Thrombosis After Injury to Atherosclerotic Vessels in Apolipoprotein E–Deficient Mice

Eitzman

Westrick

et al. 2000

ATVB

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Abstract-The increased risk of hyperlipidemia on the development of complications of atherosclerosis is well established.Cholesterol-lowering therapies lead to a decrease in the incidence of vascular thrombotic events that is out of proportion to the reduction in plaque size. This suggests that the occurrence of acute thrombosis overlying a disrupted plaque is influenced by changes in lipid levels. The influence of acute hyperlipidemia on the development of thrombosis overlying an atherosclerotic plaque in vivo has not been extensively studied. We used a murine model of vascular injury induced by a photochemical reaction to elicit thrombus formation overlying an atherosclerotic plaque. Fifteen apolipoprotein E-deficient mice were maintained on normal chow until the age of 30 weeks. Five days before the induction of thrombosis, 6 mice were started on a high fat diet, and 9 mice were continued on normal chow. Mice then underwent photochemical injury to the common carotid artery immediately proximal to the carotid bifurcation, where an atherosclerotic plaque is consistently present. Mice maintained on normal chow developed occlusive thrombi, determined by cessation of blood flow, 44Ϯ5 minutes (meanϮSEM) after photochemical injury, whereas mice fed a high fat chow developed occlusive thrombosis at 27Ϯ3 minutes (PϽ0.02). Histological analysis confirmed the presence of acute thrombus formation overlying an atherosclerotic plaque. These studies demonstrate a useful model for assessing the determinants of thrombosis in the setting of atherosclerosis and show that acute elevations in plasma cholesterol facilitate thrombus formation at sites of atherosclerosis after vascular injury. Key Words: carotid artery Ⅲ transgenic mice Ⅲ cholesterol Ⅲ plaque Ⅲ rose bengal A rterial thrombosis after plaque disruption is the critical event leading to acute vascular syndromes, including myocardial infarction, unstable angina pectoris, and stroke. 1 Elevated cholesterol levels increase the risk of arterial thrombotic events in patients with atherosclerosis, and cholesterollowering therapy reduces the risk of myocardial infarction and stroke to an extent that is out of proportion to the reduction in plaque size. 2 Alterations in lipid levels have been proposed to influence thrombosis by modifying the activity of coagulation proteins, 3,4 platelets, 5 and fibrinolytic factors. 6,7 However, the effect of acute high fat feeding-induced hypercholesterolemia on the development of occlusive thrombosis after injury to an atherosclerotic artery has not been extensively analyzed.We have developed a model of atherosclerotic plaque disruption with the use of atherosclerosis-prone mice that leads to occlusive arterial thrombosis. This model was used to analyze the effect of high fat feeding on the time to occlusive thrombosis. Methods MiceApoE-deficient (apoE Ϫ/Ϫ ) mice were purchased from Jackson Labs, Bar Harbor, Me. These mice were backcrossed to C57BL/6J mice for at least 10 generations. All mice were maintained on normal chow (PicoLab Rodent C...

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“…21 Reactive oxygen species generated in the lumen are thought to be the main contributor of endothelial damage leading to thrombosis. 22 Based on the resemblance of this process to atherosclerotic thrombosis, the method was used in many animal studies to investigate a thrombosis mechanism and to evaluate thrombosis treatment. 38 -42 The method was also used in a cerebral infarction model, in which the laser was illuminated to the whole parietal convexity.…”

Section: Discussionmentioning

confidence: 99%

“…19 Among various animal models of endothelial damage, 20,21 rose bengal injection with mild laser illumination can selectively injure ECs and is regarded as the model that best resembles thrombosis in the setting of atherosclerosis. [21][22][23] The resultant denuded segment is restricted to the area of laser illumination. 22,23 Other methods of injuring endothelium include laser injury alone, topical application of chemicals (eg, ferric chloride), and mechanical damage, which may lack specificity in injured cell types, may not result in uniform denudation, or may require direct application of the toxic chemicals onto the brain surface.…”

mentioning

confidence: 99%

“…[21][22][23] The resultant denuded segment is restricted to the area of laser illumination. 22,23 Other methods of injuring endothelium include laser injury alone, topical application of chemicals (eg, ferric chloride), and mechanical damage, which may lack specificity in injured cell types, may not result in uniform denudation, or may require direct application of the toxic chemicals onto the brain surface. 20,21 To clarify repair processes of endothelial damage and to identify responsible cells for reconstructing endothelium, we damaged ECs with the rose bengal method and evaluated time-lapse images of reendothelialization captured through the cranial window.…”

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confidence: 99%

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Resident Endothelial Cells Surrounding Damaged Arterial Endothelium Reendothelialize the Lesion

Itoh

Toriumi

Yamada

et al. 2010

ATVB

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Objective-To evaluate endothelial repair processes in denuded pial vessels to clarify mechanisms for reconstructing endothelium (because endothelial repair of the cerebral artery after its damage is critical for the prevention of thrombosis, the maintenance of vascular tone, and the protection of the brain by the blood-brain barrier). Methods and Results-Endothelial cells (ECs) in a 350-m-long segment of the middle cerebral artery were damaged through a photochemical reaction. Tie2-green fluorescent protein transgenic mice were used for the identification of ECs. Six hours after the endothelial damage, ECs were detached from the luminal surface of the damaged artery, which was then covered with a platelet carpet. Within 24 hours, recovery of the denuded artery started at both edges, with EC elongation and migration. The repair rate was faster at the proximal edge than at the distal edge. Reendothelialization with EC proliferation peaked at 2 to 3 days and ended at 5 days, together with normalization of EC length, with no apparent involvement of foreign progenitor cells. Conclusion-Our in vivo study demonstrated a stepwise reendothelialization process by resident ECs of the pial artery.The prevention of thrombosis, vasospasm, and treatment for blood-brain barrier dysfunction should be considered during the reendothelialization period. Key Words: Tie2 Ⅲ reendothelialization Ⅲ pial artery Ⅲ confocal laser microscopy Ⅲ photochemical reaction B ecause endothelial damage and subsequent exposure of subendothelial tissue in the cerebral artery quickly induces a luminal thrombus and disturbs cerebral blood flow, urgent endothelial repair is critical to minimize ischemic damage, especially after rupture of an atherosclerotic plaque, commonly observed at the carotid artery and the intracranial cerebral arteries. Reendothelialization is also essential to recover normal vascular tone controlled by vasodilatory mediators, such as nitric oxide released from the endothelium. Furthermore, loss of the endothelial tight junction results in breakdown of the blood-brain barrier, causing vasogenic edema. Therefore, restoration of endothelial function in the cerebral vessel is an urgent process for the brain.Endothelial damage of the cerebral artery is a key mechanism involved in the pathophysiology of various brain diseases, including stroke, atherosclerosis, 1 diabetes mellitus, 2 dyslipidemia, 3 hypertension, 4 vasculitis, 5 multiple sclerosis, 6 radiation necrosis, 7 and drug adverse effects. 8 Some markers of endothelial damage are good indicators for the future incidence of cardiovascular events, including stroke. 9 Carotid endarterectomy, a treatment for carotid stenosis, removes atheroma and endothelial cells (ECs), exposing subendothelial tissue. 10 In these conditions, endothelial repair is one of the major targets of treatment.Histological evaluation of reendothelialization and neointima formation after mechanical carotid denudation was previously reported. 11-13 However, the dynamic and minute process of endothelial repair...

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Singlet oxygen and myocardial injury: Ultrastructural, cytochemical and electrocardiographic consequences of photoactivation of rose bengal

Cited by 73 publications

References 28 publications

Homozygosity for Factor V Leiden Leads to Enhanced Thrombosis and Atherosclerosis in Mice

Homozygosity for Factor V Leiden Leads to Enhanced Thrombosis and Atherosclerosis in Mice

Hyperlipidemia Promotes Thrombosis After Injury to Atherosclerotic Vessels in Apolipoprotein E–Deficient Mice

Resident Endothelial Cells Surrounding Damaged Arterial Endothelium Reendothelialize the Lesion

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