Disturbance during foetal period behind severe eye disease

August 6, 2012

(Medical Xpress) -- The congenital eye disease persistent foetal vasculature syndrome leads to bleeding, detached retina, and a cloudy lens. Now researchers at Uppsala University show in a model for the disease that it may be associated with an excessive expression of a growth factor during the foetal period.

During the foetal period, temporary blood vessels, so-called hyaloid vessels, play an important role for the development of the eye. In normal foetal development these blood vessels regress and disappear apace with the formation of the retina’s real blood vessels. If the regression of the temporary blood vessels does not take place, defects arise in the eye, leading to the uncommon but severe disease persistent foetal vasculature syndrome, PFVS.

In a study published by the scientific journal PLoS ONE researchers at Uppsala University in Sweden and the University of Murcia in Spain show that the disease can be linked to disturbances in growth signals during the foetal period.

"The symptoms result from an excess of the PDGF, which prevents the temporary blood vessels of the foetal stage from disappearing, which in turn prevents normal development of blood vessels in the retina," says Karin Forsberg Nilsson, professor at the Department of Immunology, Genetics and Pathology at the Rudbeck Laboratory, who directed the study.

The finding is based on studies of mice with altered levels of the growth factor PDGF in neural  stem cells, which play a key role in the development of the eye. In mice with an altered level of the growth factor, there was no regression of the temporary . Instead major defects arose during retina development including severely impaired blood-vessel development. The symptoms could be alleviated when the growth factor was blocked.

"In humans PFVS can lead to bleeding in the eye – because the vessels leak, cloudy lens – so-called cataract, and . We see major similarities with the disease," says Karin Forsberg-Nilsson.

These finding means that there is now a model for studying the in greater detail, which can lead to more effective treatment.

Explore further: Gene found in humans, mice protects cornea transparency

More information: dx.plos.org/10.1371/journal.pone.0042488

Related Stories

Gene found in humans, mice protects cornea transparency

December 12, 2011

A transparent cornea is essential for vision, which is why the eye has evolved to nourish the cornea without blood vessels. But for millions of people around the world, diseases of the eye or trauma spur the growth of blood ...

Recommended for you

Vitamin B3 prevents glaucoma in laboratory mice

February 16, 2017

In mice genetically predisposed to glaucoma, vitamin B3 added to drinking water is effective at preventing the disease, a research team led by Jackson Laboratory Professor and Howard Hughes Medical Investigator Simon W.M. ...

GARP2 accelerates retinal degeneration in a mouse model

February 15, 2017

In the retina of the eye, rod and cone cells turn light into electrical signals, the first step toward human vision. University of Alabama at Birmingham researchers are studying rod cell proteins GARP1 and GARP2 to learn ...

Myopia cell discovered in retina

February 6, 2017

Northwestern Medicine scientists have discovered a cell in the retina that may cause myopia when it dysfunctions. The dysfunction may be linked to the amount of time a child spends indoors and away from natural light.

0 comments

Please sign in to add a comment. Registration is free, and takes less than a minute. Read more

Click here to reset your password.
Sign in to get notified via email when new comments are made.