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JCI table of contents: Aug. 16, 2007
Date:8/16/2007

3764; Fax: (615) 343-4704; E-mail: breyerma@lilly.com.

Youfei Guan Peking University Health Science Center, Beijing, People's Republic of China. Phone: 86-10-8280-1447; Fax: 86-10-8280-1447; E-mail: youfeiguan@bjmu.edu.cn.

View the PDF of this article at: https://www.the-jci.org/article.php?id=29838


OPHTHALMOLOGY: Eyeing up a role for S1P2R in abnormal blood vessel formation

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
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Journal of Clinical Investigation
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