A thrombin inhibitor reduces brain edema, glioma mass and neurological deficits in a rat glioma model

Hua, Ya; Keep, Richard F.; Hoff, Julian T.; Xi, Guan

doi:10.1007/978-3-7091-0651-8_103

Cited by 25 publications

(24 citation statements)

References 21 publications

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“…G-protein-coupled receptors (GPCRs) 6 constitute the largest class of cell surface receptors, but the involvement of GPCR signaling in regulating glial tumor growth has not been explored extensively. Thrombin, a peptide hormone and GPCR ligand, is detected in cancer cells, including glioblastoma (1)(2)(3)(4)(5), and enhanced signaling through the PAR-1 thrombin receptor has been reported to cause cell transformation and to increase tumor cell invasiveness (6 -8). One proposed transduction mechanism by which PAR-1 receptor stimulation leads to enhanced proliferation is through activation of the low molecular weight G-protein RhoA (9 -11).…”

Section: Rap1 Is a Ras Family Gtpase With A Well Documented Role In Ementioning

confidence: 99%

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The Ras-related Protein, Rap1A, Mediates Thrombin-stimulated, Integrin-dependent Glioblastoma Cell Proliferation and Tumor Growth

Sayyah

Bartáková

Nogal

et al. 2014

Journal of Biological Chemistry

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Section: Rap1 Is a Ras Family Gtpase With A Well Documented Role In Ementioning

confidence: 99%

“…2 Supported by National Institutes of Health Grant R01 CA107263. 3 Supported by National Institutes of Health Grants GM 36927 and R37HLO28143. 4 Supported by U. S. Department of Defense Award W81XWH1110355.…”

Section: Rap1 Is a Ras Family Gtpase With A Well Documented Role In Ementioning

confidence: 99%

The Ras-related Protein, Rap1A, Mediates Thrombin-stimulated, Integrin-dependent Glioblastoma Cell Proliferation and Tumor Growth

Sayyah

Bartáková

Nogal

et al. 2014

Journal of Biological Chemistry

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“…The development of cerebral edema has a stronger temporal association with neurologic deterioration in the autologous blood injection model compared with the collagenase model, and is slower and more protracted in human compared with experimental ICH (Butcher et al, 2004;Gebel et al, 2002a;Hua et al, 2003;Qureshi et al, 2009;Rosenberg et al, 1990;Yang et al, 1994)-as is red cell resorption (Butcher et al, 2004;MacLellan et al, 2008;Xi et al, 2006). Further, when matched for hematoma size, the total loss of brain tissue can be twice as much in the collagenase model compared with the blood injection model (MacLellan et al, 2008).…”

Section: Pathophysiologymentioning

confidence: 99%

Experimental Intracerebral Hemorrhage: Avoiding Pitfalls in Translational Research

Kirkman

Allan

Parry‐Jones

2011

J Cereb Blood Flow Metab

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Intracerebral hemorrhage (ICH) has the highest mortality of all stroke subtypes, yet treatments are mainly limited to supportive management, and surgery remains controversial. Despite significant advances in our understanding of ICH pathophysiology, we still lack preclinical models that accurately replicate the underlying mechanisms of injury. Current experimental ICH models (including autologous blood and collagenase injection) simulate different aspects of ICH-mediated injury but lack some features of the clinical condition. Newly developed models, notably hypertension-and oral anticoagulant therapy-associated ICH models, offer added benefits but further study is needed to fully validate them. Here, we describe and discuss current approaches to experimental ICH, with suggestions for changes in how this condition is studied in the laboratory. Although advances in imaging over the past few decades have allowed greater insight into clinical ICH, there remains an important role for experimental models in furthering our understanding of the basic pathophysiologic processes underlying ICH, provided limitations of animal models are borne in mind. Owing to differences in existing models and the failed translation of benefits in experimental ICH to clinical practice, putative neuroprotectants should be trialed in multiple models using both histological and functional outcomes until a more accurate model of ICH is developed.

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“…This observation may be worth being pursued within a prospective trial. Other experimental treatments directed against peritumoral edema have only been assessed in preclinical studies: argatroban, a thrombin antagonist, reduced the peritumoral edema in a rodent glioma model [72]. Glyburide, a well-known antidiabetic drug, inhibits the sulfonylurea receptor 1 and reduced cerebral metastasis-related edema in rats [73].…”

Section: Other Agentsmentioning

confidence: 99%

Tumor-associated edema in brain cancer patients: pathogenesis and management

Roth

Regli

Tonder

2013

Expert Review of Anticancer Therapy

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The long-term treatment of peritumoral edema remains a major challenge in clinical neurooncology. Steroids have been and will remain the backbone of any anti-edematous therapy because of their striking activity, convenient oral administration and also because of their cost-effectiveness. Their side effects, however, can compromise quality of life, particularly upon continuous administration. Therapeutic alternatives which may replace or -at least -help to reduce the steroid dose are limited. However, with the development of new agents such as corticorelin acetate, there is a hope that steroid-induced side effects can be delayed and reduced. The administration of anti-angiogenic agents with steroid-sparing effects, for example, bevacizumab, is limited due to their costs. Increased knowledge on boswellic acids and cyclooxygenase-2 inhibitors which are available for clinical application may help to exploit their anti-edema activity more efficiently in the future.

show abstract

A thrombin inhibitor reduces brain edema, glioma mass and neurological deficits in a rat glioma model

Cited by 25 publications

References 21 publications

The Ras-related Protein, Rap1A, Mediates Thrombin-stimulated, Integrin-dependent Glioblastoma Cell Proliferation and Tumor Growth

The Ras-related Protein, Rap1A, Mediates Thrombin-stimulated, Integrin-dependent Glioblastoma Cell Proliferation and Tumor Growth

Experimental Intracerebral Hemorrhage: Avoiding Pitfalls in Translational Research

Tumor-associated edema in brain cancer patients: pathogenesis and management

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