Many millions of individuals worldwide suffer from vision loss as a result of the formation of an abnormal network of blood vessels in the eye. This abnormal blood vessel network forms in response to damage to the retina and often occurs in individuals who are diabetic. Understanding the molecular mechanisms controlling the development of the network of blood vessels in the retina under normal and pathological conditions is therefore an area of intensive research.
In a study appearing online on August 16, in advance of publication in the September print issue of the Journal of Clinical Investigation, Timothy Hla and colleagues from the University of Connecticut School of Medicine, Farmington, show that under normal conditions, blood vessel development is indistinguishable in wild-type mice and in mice lacking a protein known as sphingosine -1-phosphate receptor 2 (S1P2R). By contrast, damage to the retina, in the form of low levels of oxygen, induces the formation of an abnormal network of blood vessels in the eyes of wild-type mice, but not in the eyes of S1P2R-deficient mice.
The absence of pathological blood vessel formation in S1P2R-deficient mice was associated with decreased inflammatory cell infiltration of the retina and decreased expression of the proinflammatory enzyme cyclooxygenase-2. This demonstration that S1P2R-driven inflammation is an important event in pathological blood vessel formation in the eye led the authors to suggest that inhibiting S1P2R activation in the retina might provide a new therapeutic approach to treating diseases of the eye caused by the presence of an abnormal blood vessel network.
Article: Essential role of sphingosine -1- phosphate receptor 2 in pathological angiogenesis of the mouse retina
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