Blood is thicker than lymph
Mark L. Kahn
Mark L. Kahn
Published December 20, 2007
Citation Information: J Clin Invest. 2008;118(1):23-26. https://doi.org/10.1172/JCI34485.
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Commentary

Blood is thicker than lymph

Abstract

Growth of blood and lymphatic vessels is essential in the developing embryo and in the pathogenesis of human diseases such as cancer, but the signaling pathways that regulate vessel growth and function are not yet well characterized. In this issue of the JCI, studies by Fritz-Six et al. and Ichikawa-Shindo et al. demonstrate that loss of signaling by the adrenomedullin peptide results in embryonic edema and death (see the related articles beginning on pages 40 and 29, respectively). Remarkably, this phenotype is attributed to defects in lymphatic vessels by one group and to defects in blood vessels by the other. In addition to defining what I believe to be a novel angiogenic signaling pathway, these studies demonstrate the intricate molecular, genetic, and physiologic relationships between blood and lymphatic vessels that must be considered by investigators of vascular biology.

Authors

Mark L. Kahn

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Figure 1

Development of edema due to loss of AM signaling.

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Development of edema due to loss of AM signaling. As reported by Fritz-S...
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).