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Mark L. Kahn
Published in Volume 118, Issue 1
J Clin Invest. 2008; 118(1):23–26 doi:10.1172/JCI34485
Abstract | Full text | PDF
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Figure 1
Development of edema due to loss of AM signaling.

As reported by Fritz-Six et al. (6) and Ichikawa-Shindo et al. (7) in this issue of the JCI, the massive edema observed in midgestation mouse embryos lacking AM signaling is caused by a combination of fluid and protein leakage from blood vessels due to altered vascular permeability (top panels) and reduced lymphatic uptake of extravasated fluid and protein due to reduced lymphatic vessel growth (bottom panels). In both blood and lymphatic vessels, AM signaling is mediated by Calcrl-Ramp2 receptor complexes expressed on endothelial cells. Arrows indicate the movement of fluid in response to hydrostatic pressure (an outward force in blood capillaries) and osmotic pressure (an inward force in blood capillaries).