Identification of a novel source of progenitor cells that form arterial valve leaflets and that, when disrupted, can lead to bicuspid arterial valve, the most common human cardiac malformation.

Arterial myocyte PKD2 channels are activated by vasoconstrictor stimuli, which increases blood pressure, are upregulated during hypertension and cell-specific knockout in vivo reduces both physiological blood pressure and hypertension.

Transcriptome analysis reveals an alternative splicing program induced in the arterial endothelium under low-flow inflammatory conditions by platelet and macrophage recruitment and dependent upon the RNA-binding splice factor Rbfox2.

The kinase JNK is required in endothelial cells for the development of native collateral arteries.

Second-order guidance, a novel mechanism by which an initial guidance cue controls expression of a second guidance receptor, is required for precise refinement of axon trajectories during PNS development.

The transcription factor GATA6 selects the embryonic vessels that will be reorganized into the major thoracic arteries by promoting local differentiation of vascular smooth muscle cells.

The response of the brainstem to increased levels of carbon dioxide in the blood is coordinated with the response of the cardiovascular system.

CO₂/H⁺-dependent purinergic signaling by astrocytes provides specialized control of vascular tone in a brainstem respiratory center in a manner that contributes to respiratory behavior.

A multi-pronged approach shows that a G_s-coupled purinergic receptor is a sensor for glucose-mediated, PKA-dependent potentiation of vascular L-type calcium channels and vasoconstriction.

Flow-dependent remodeling of blood vessels is critical for normal physiology and for recovery from arterial blockage in disease; understanding its cellular mechanisms may lead to the development of treatments for patients that are deficient in this process following myocardial infarction or other vascular diseases.