Scientists have been wrestling with the "clarity" puzzle for many decades. And, while some previous studies have revealed small clues, none have pointed to one major mechanism, until this study.
In most other tissues of the body, blood vessel growth or angiogenesis occurs in response to a need for increased blood flow to heal an injured or infected area. The immune system sends in growth factors such as vascular endothelial growth factor (VEGF) to bind with a protein receptor called VEGFR-2 on blood vessels to trigger vessel growth. Three forms of VEGF--A, C, and D--bind with this receptor. Two of them, C and D also bind with VEGFR-3, which is usually found on cells lining lymphatic vessels, to stimulate the growth of lymphatic vessels.
Dana's team began to suspect the involvement of VEGFR-3 in stopping blood growth in corneas when they noticed unexpectedly that large amounts of the protein seemed to exist naturally on healthy corneal epithelium, a previously unknown location for the receptor. Dana and his team were already aware from clinical experience that the epithelium most likely played a role in suppressing blood vessel growth on the cornea, having witnessed blood vessels develop on corneas stripped of their epithelial layers.
They began to theorize that the large amounts of VEGFR-3, in this new, non-vascular location, might be attracting and sucking up all the C and D VEGF growth factors, thereby blocking them from binding with VEGFR-2. And, because this binding took place in a non-vascular setting, the growth factors were neutralized.
To test their theory, the team conducted a series of experimen
'"/>
Source:Schepens Eye Research Institute