Local administration of AD.VEGF-A165 to the utero-placental circulation reduces brain sparing and may enhance fetal growth in an FGR model of guinea pig pregnancy

Mehta, Vikas; Boyd, Michael; Barker, H; Avdic-Belltheus, Adnan; Carr, David; Martin, J. N.; Zachary, I; Peebles, DM; David, AL

doi:10.1136/fetalneonatal-2012-301809.22

Cited by 2 publications

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“…Increased fetal growth velocity was confirmed in a second experimental group, administering overnourished adolescent dams uterine artery injections of either Ad.VEGF or saline . Results from treatment in FGR guinea pig pregnancy suggest a similar improvement in fetal growth velocity …”

Section: How Can We Treat Poor Placentation?mentioning

confidence: 84%

Treatment of poor placentation and the prevention of associated adverse outcomes – what does the future hold?

2014

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Poor placentation, which manifests as pre-eclampsia and fetal growth restriction, is a major pregnancy complication. The underlying cause is a deficiency in normal trophoblast invasion of the spiral arteries, associated with placental inflammation, oxidative stress, and an antiangiogenic state. Peripartum therapies, such as prenatal maternal corticosteroids and magnesium sulphate, can prevent some of the adverse neonatal outcomes, but there is currently no treatment for poor placentation itself. Instead, management relies on identifying the consequences of poor placentation in the mother and fetus, with iatrogenic preterm delivery to minimise mortality and morbidity. Several promising therapies are currently under development to treat poor placentation, to improve fetal growth, and to prevent adverse neonatal outcomes. Interventions such as maternal nitric oxide donors, sildenafil citrate, vascular endothelial growth factor gene therapy, hydrogen sulphide donors, and statins address the underlying pathology, while maternal melatonin administration may provide fetal neuroprotection. In the future, these may provide a range of synergistic therapies for pre-eclampsia and fetal growth restriction, depending on the severity and gestation of onset.

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Section: How Can We Treat Poor Placentation?mentioning

confidence: 84%

Treatment of poor placentation and the prevention of associated adverse outcomes – what does the future hold?

2014

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“…There is also a reduction in available maternal VEGF and an increase in its soluble receptor, soluble fms-like tyrosine kinase 1 (sFlt1) (61,62). Our research over the last eight years has demonstrated that adenovirus vector (Ad) mediated manipulation of VEGF expression in the uterine arteries produces an increase in uterine artery blood flow (63)(64)(65) and ameliorates the effects of FGR in animal models (66,67).…”

Section: Fetal Growth Restrictionmentioning

confidence: 99%

Gene Therapy for Obstetric Conditions

Spencer

Carr

David

2014

Fet. Matern. Med. Rev.

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The first clinical trials of gene therapy in the 1990s offered the promise of a new paradigm for the treatment of genetic diseases. Over the decades that followed the challenges and setbacks which gene therapy faced often overshadowed any successes. Despite this, recent years have seen cause for renewed optimism. In 2012 Glybera™, an adeno-associated viral vector expressing lipoprotein lipase, became the first gene therapy product to receive marketing authorisation in Europe, with a licence to treat familial lipoprotein lipase deficiency. This followed the earlier licensing in China of two gene therapies: Gendicine™ for head and neck squamous cell carcinoma and Oncorine™ for late-stage nasopharyngeal cancer. By this stage over 1800 clinical trials had been, or were being, conducted worldwide, and the therapeutic targets had expanded far beyond purely genetic disorders. So far no trials of gene therapy have been carried out in pregnancy, but an increasing understanding of the molecular mechanisms underlying obstetric diseases means that it is likely to have a role to play in the future. This review will discuss how gene therapy works, its potential application in obstetric conditions and the risks and limitations associated with its use in this setting. It will also address the ethical and regulatory issues that will be faced by any potential clinical trial of gene therapy during pregnancy.

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Local administration of AD.VEGF-A165 to the utero-placental circulation reduces brain sparing and may enhance fetal growth in an FGR model of guinea pig pregnancy

Cited by 2 publications

References 0 publications

Treatment of poor placentation and the prevention of associated adverse outcomes – what does the future hold?

Treatment of poor placentation and the prevention of associated adverse outcomes – what does the future hold?

Gene Therapy for Obstetric Conditions

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