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The angiopoietin-Tie signaling pathway has long been known to be essential for the maturation and maintenance of healthy blood vessels. It stabilizes the vessel wall and regulates vascular growth during development. At the same time, it plays an important role in inflammation, when blood vessels become activated and immune cells leave the bloodstream and enter the surrounding tissue. How the same signaling pathway can control such different biological functions has remained unclear.

A team led by Dr. Mahak Singhal and Dr. Hellmut Augustin has now found an answer to this question. At the center of the discovery is the vascular receptor Tie1, a protein found almost exclusively on endothelial cells—the cells lining the inner surface of blood vessels. During inflammation, part of the Tie1 receptor is enzymatically cleaved from the cell surface.

To investigate the significance of this process, the researchers generated genetically modified mice in which Tie1 can no longer be cleaved. The animals developed entirely normal blood vessels and showed no detectable abnormalities during development, adulthood or aging. Even under conditions that normally stimulate the formation of new blood vessels, vascular growth remained unchanged.

The picture was different when the mice were exposed to inflammatory stimuli. The genetically modified animals showed a markedly reduced inflammatory response. Their blood vessels were less strongly activated, and substantially fewer immune cells migrated from the bloodstream into the surrounding tissue.

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