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Genetic lineage tracing reveals the cardiopharyngeal mesoderm as a cellular origin of craniofacial and cardiac lymphatic vessels, which most often affected in lymphatic malformation patients.

Three-dimensional imaging was used to identify structural and quantitative features of developing lymphatics in the kidneys of mice, humans and in a genetic mouse model of polycystic kidney disease.

A novel molecular strategy to block transcription factor activity using small molecule interference of multiple protein-protein interactions is reported.

The sphingosine 1-phosphate receptor-1 (S1PR1) signals in heterogenous populations of mouse adventitial lymphatic (LEC) and arterial endothelial cells (aEC1, aEC2) to regulate chromatin and the transcriptome, thus affecting their phenotypes.

While Dectin-1 is a well-known C-type lectin receptor recognizing b-glucan and involved in anti-fungal immunity, human Dectin-1 is O-glycosylated and acts as a ligand for another C-type lectin receptor, CLEC-2, expressed by platelets that mediates homeostatic responses such as lymphangiogenesis.

In mouse cardiomyocytes, (lymph)angiogenic growth factors are induced during early hypoxia by a translational mechanism involving a new IRES trans-acting factor, vasohibin-1.

A small molecule called Sm4 can disrupt interactions involving a transcription factor called Sox18, while having little impact on other members of the SoxF family.

The lymphatic and blood network of the mouse epididymis in adulthood and during postnatal ontogeny has been analyzed in detail.

Genetic and molecular analyses show that FOXC1 and FOXC2 play a role in controlling lymphatic valve maintenance as key mediators of mechanotransduction to control cytoskeletal organization and RhoA/ROCK signaling.

Identification of a developmental mechanism critical for the generation of brain vessel heterogeneity.