The Mouse Arteriovenous Fistula Model

Yang, Binxia; Shergill, Uday; Fu, Alex A.; Knudsen, Bruce E.; Misra, Sanjay

doi:10.1016/j.jvir.2009.03.044

Cited by 39 publications

(50 citation statements)

References 20 publications

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“…However, unfortunately, to date this has not translated into many robust clinical trials that have evaluated innovative and novel therapies (80) or resulted in effective therapies available for our hemodialysis patients. Further advancements that translate our understanding of neointimal hyperplasia development and vascular remodeling in hemodialysis access dysfunction into therapies will require multidisciplinary efforts that use the advancements from animal studies of AVF and AVG (22,53,63,81), use of innovative and cutting edge technology in areas such as genomics, high-resolution imaging, nanomaterials, and bioengineering, and collaborative efforts with the biomedical industry to invest in promising targets to develop these therapies. In a broader context, AVFs and AVGs may be the ideal clinical model to test future novel therapies for neointimal hyperplasia and vascular remodeling in other areas of vascular disease (e.g., coronary artery disease and bypass grafts, peripheral arterial disease, and postangioplasty restenosis) because of the superficial location of the vessels, the frequency of accessing the vessels, the aggressiveness of the vascular lesion, and the fact that hemodialysis patients are a captive audience because they undergo dialysis three times a week (4,82).…”

Section: Discussionmentioning

confidence: 99%

New Insights into Dialysis Vascular Access: Molecular Targets in Arteriovenous Fistula and Arteriovenous Graft Failure and Their Potential to Improve Vascular Access Outcomes

Lee

Misra

2016

CJASN

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Vascular access dysfunction remains a major cause of morbidity and mortality in hemodialysis patients. At present there are few effective therapies for this clinical problem. The poor understanding of the pathobiology that leads to arteriovenous fistula (AVF) and graft (AVG) dysfunction remains a critical barrier to development of novel and effective therapies. However, in recent years we have made substantial progress in our understanding of the mechanisms of vascular access dysfunction. This article presents recent advances and new insights into the pathobiology of AVF and AVG dysfunction and highlights potential therapeutic targets to improve vascular access outcomes.

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Section: Discussionmentioning

confidence: 99%

New Insights into Dialysis Vascular Access: Molecular Targets in Arteriovenous Fistula and Arteriovenous Graft Failure and Their Potential to Improve Vascular Access Outcomes

Lee

Misra

2016

CJASN

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“…Four weeks later, a carotid artery to jugular vein AVF was created (Fig. 1) [5, 6]. The shRNA for Vegf-A was purchased from Open Biosystems (Huntsville, AL) and it was prepared according to the manufacturer's protocol [7].…”

Section: Methodsmentioning

confidence: 99%

“…The vessels were homogenized and the RNA was isolated using RNeasy mini kit (Qiagen) [5, 6]. The gene expression of interest was determined using RT-PCR analysis [6]. The primers used are listed in Table 1.…”

Section: Methodsmentioning

confidence: 99%

The Role of Repeat Administration of Adventitial Delivery of Lentivirus-shRNA-Vegf-A in Arteriovenous Fistula to Prevent Venous Stenosis Formation

Janardhanan¹,

Yang²,

Kilari³

et al. 2016

Journal of Vascular and Interventional Radiology

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Purpose Previous study has demonstrated that adventitial delivery of lentivirus mediated Vegf-A shRNA (LV-shRNA-Vegf-A, small hairpin RNA that inhibits Vegf-A gene expression) at the time of arteriovenous fistula (AVF) creation increases the lumen vessel area (LVA) of the outflow vein and reduces venous neointimal hyperplasia (VNH). However, the effect of decreasing Vegf-A and improving LVA decreases by 2-weeks as stenosis develops. The aim of the present study was to determine if a second dose of LV-shRNA-Vegf-A could improve LVA and decrease VNH. Methods Chronic kidney disease was created in C57BL/6 mice and 28 days later, a AVF was created by connecting right carotid artery to ipsilateral jugular vein. 5×106 plaque forming units of LV-shRNA-Vegf-A or control shRNA was administered to the adventitia of the outflow vein immediately after AVF creation and a second dose of the same treatment fourteen days later. Animals were sacrificed at 21, 28, and 42 days after AVF creation for reverse transcription polymerase chain reaction (RT-PCR) and histomorphometric analyses. Results By day 21, there was a 25% increase in the average LVA (day 21: P=0.11), with a decrease in cell proliferation (day 21: P=0.0079, day 28: P=0.28; day 42: P=0.5), decrease in α-smooth muscle cell actin staining (day 21: P<0.0001, day 28: P<0.05; day 42: P=0.59), and decrease in hypoxic stress (day 21: P<0.001, day 28: P=0.28; day 42: P=0.46) in LV versus control shRNA vessels, respectively. Conclusion A second dose of LV-shRNA-Vegf-A administration results in a moderate improvement in LVA at day 21.

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“…Furthermore, the experimental construct could also be further adapted to the study of other cerebrovascular diseases related with venous hypertension such as migraine, transient global amnesia, transient monocular blindness, etc. 11 However, previous attempts to construct these mice models have demonstrated the difficulties with patency of the fistula due to the diminutive anatomy 5,12 . Here, we describe our step-by-step protocol for a successful anastomosis of the murine CCA and EJV that translates into a long-term patent fistula and a durable venous hypertension in the mouse.…”

Section: Introductionmentioning

confidence: 99%

Adult Mouse Venous Hypertension Model: Common Carotid Artery to External Jugular Vein Anastomosis.

Yang

Rodríguez-Hernández

Walker

et al. 2015

JoVE

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The understanding of the pathophysiology of brain arteriovenous malformations and arteriovenous fistulas has improved thanks to animal models. A rat model creating an artificial fistula between the common carotid artery (CCA) and the external jugular vein (EJV) has been widely described and proved technically feasible. This construct provokes a consistent cerebral venous hypertension (CVH), and therefore has helped studying the contribution of venous hypertension to formation, clinical symptoms, and prognosis of brain AVMs and dural AVFs. Equivalent mice models have been only scarcely described and have shown trouble with stenosis of the fistula. An established murine model would allow the study of not only pathophysiology but also potential genetic therapies for these cerebrovascular diseases. We present a model of arteriovenous fistula that produces a durable intracranial venous hypertension in the mouse. Microsurgical anastomosis of the murine CCA and EJV can be difficult due to diminutive anatomy and frequently result in a non-patent fistula. In this step-by-step protocol we address all the important challenges encountered during this procedure. Avoiding excessive retraction of the vein during the exposure, using 11-0 sutures instead of 10-0, and making a carefully planned end-to-side anastomosis are some of the critical steps. Although this method requires advanced microsurgical skills and a longer learning curve that the equivalent in the rat, it can be consistently developed. This novel model has been designed to integrate transgenic mouse techniques with a previously well-established experimental system that has proved useful to study brain AVMs and dural AVFs. By opening the possibility of using transgenic mice, a broader spectrum of valid models can be achieved and genetic treatments can also be tested. The experimental construct could also be further adapted to the study of other cerebrovascular diseases related with venous hypertension such as migraine, transient global amnesia, transient monocular blindness, etc.

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The Mouse Arteriovenous Fistula Model

Cited by 39 publications

References 20 publications

New Insights into Dialysis Vascular Access: Molecular Targets in Arteriovenous Fistula and Arteriovenous Graft Failure and Their Potential to Improve Vascular Access Outcomes

New Insights into Dialysis Vascular Access: Molecular Targets in Arteriovenous Fistula and Arteriovenous Graft Failure and Their Potential to Improve Vascular Access Outcomes

The Role of Repeat Administration of Adventitial Delivery of Lentivirus-shRNA-Vegf-A in Arteriovenous Fistula to Prevent Venous Stenosis Formation

Adult Mouse Venous Hypertension Model: Common Carotid Artery to External Jugular Vein Anastomosis.

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