Seminars in Thrombosis, Thrombolysis and Vascular Biology

Rc, Becker

doi:10.1159/000174860

Cited by 12 publications

(9 citation statements)

References 11 publications

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“…The FBs are the main cells in the tunica adventitia. A large number of studies have demonstrated that vascular cells play a critical role in maintaining the normal functions of blood vessels . According to the basic principle of tissue engineering, vascular cells are the initial candidates for vascular regeneration.…”

Section: Terminally Differentiated Vascular Cellsmentioning

confidence: 99%

Cell‐based strategies for vascular regeneration

Zou

Fan

Fartash

et al. 2016

J Biomedical Materials Res

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Vascular regeneration is known to play an essential role in the repair of injured tissues mainly through accelerating the repair of vascular injury caused by vascular diseases, as well as the recovery of ischemic tissues. However, the clinical vascular regeneration is still challenging. Cell-based therapy is thought to be a promising strategy for vascular regeneration, since various cells have been identified to exert important influences on the process of vascular regeneration such as the enhanced endothelium formation on the surface of vascular grafts, and the induction of vessel-like network formation in the ischemic tissues. Here are a vast number of diverse cell-based strategies that have been extensively studied in vascular regeneration. These strategies can be further classified into three main categories, including cell transplantation, construction of tissue-engineered grafts, and surface modification of scaffolds. Cells used in these strategies mainly refer to terminally differentiated vascular cells, pluripotent stem cells, multipotent stem cells, and unipotent stem cells. The aim of this review is to summarize the reported research advances on the application of various cells for vascular regeneration, yielding insights into future clinical treatment for injured tissue/organ.

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Section: Terminally Differentiated Vascular Cellsmentioning

confidence: 99%

Cell‐based strategies for vascular regeneration

Zou

Fan

Fartash

et al. 2016

J Biomedical Materials Res

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“…Further, both experimental and clinical observations have demonstrated a major role of platelets in the pathophysiology of thrombotic states and vascular diseases (Becker 1991; Gori 2011; Kaliman et al 1983) and there is a link between platelet activation, arrhythmogenesis and sudden death (Flores 1996). Moreover, platelets are involved in the pathobiology of myocardial ischemia, infarction and hypertension (Fuster et al 1992).…”

Section: Introductionmentioning

confidence: 99%

Glycine reduces platelet aggregation

et al. 2012

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It has been demonstrated that a wide variety of white blood cells and macrophages (i.e. Kupffer cells, alveolar and peritoneal macrophages and neutrophils) contain glycine-gated chloride channels. Binding of glycine on the receptor stimulates Cl− influx causing membrane hyperpolarization that prevents agonist-induced influx of calcium. Since platelet-aggregation is calcium-dependent, this study was designed to test the hypothesis that glycine would inhibit platelet aggregation. Rats were fed diets rich of glycine for 5 days, while controls received isonitrogenous valine. The bleeding time and ADP- and collagen-induced platelet aggregation were measured. Dietary glycine significantly increased bleeding time about two fold compared to valine-treated controls. Furthermore, the amplitude of platelet aggregation stimulated with ADP or collagen was significantly decreased in whole blood drawn from rats fed 2.5 or 5 % dietary glycine by over 50 %. Addition of glycine in vitro (1–10 mM) also blunted rat platelet aggregation in a dose-dependent manner. Strychnine, a glycine receptor antagonist, abrogated the inhibitory effect of glycine on platelet-aggregation in vitro suggesting the glycine works via a glycine receptor. Glycine also blunted aggregation of human platelets. Further, the glycine receptor was detected in both rat and human platelets by western blotting. Based on these data, it is concluded that glycine prevents aggregation of platelets in a dose-dependent manner via mechanisms involving a glycine receptor.

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“…In our model, the pulmonary hypertension continued for 6-8 h. The reduction of PAP after pulmonary embolization occurred by focal vascular recanalization. Recently, it has become clear that the vas cular endothelium not only acts as a mechanical barrier but is also organ saving with a vital role in vasomotor and thromboresistance, and is influenced by vasoactive com pounds such as prostacyclin and endothelium-derived relaxing factor [10,11].…”

Section: Discussionmentioning

confidence: 99%

Canine Pulmonary Hypertension Model Induced by Pulmonary Artery Embolization of Gelatin Sponges

Yamamoto

Kawahara²,

Takahashi³

et al. 1995

Respiration

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We attempted to develop a pulmonary hypertension model in dogs by gelatin sponge embolization. We then monitored right-ventricular pressure overload by echocardiography. Gelatin sponges (Spongel®, Yamanouchi, Tokyo) were homogenized and mixed in normal saline (0.6 mg/ml). The mixture was administered via the jugular vein to general pulmonary emboli. Repeated administration of the sponges increased the mean pulmonary arterial pressure and caused right ventricular pressure overload. The degree of pulmonary hypertension was proportional to the volume of gelatin sponge injected. Echocardiography, performed both before and after embolization, proved useful assessing for the degree of right-ventricular pressure overload.

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Seminars in Thrombosis, Thrombolysis and Vascular Biology

Cited by 12 publications

References 11 publications

Cell‐based strategies for vascular regeneration

Cell‐based strategies for vascular regeneration

Glycine reduces platelet aggregation

Canine Pulmonary Hypertension Model Induced by Pulmonary Artery Embolization of Gelatin Sponges

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