Vagal Regulation of Group 3 Innate Lymphoid Cells and the Immunoresolvent PCTR1 Controls Infection Resolution
Immunity
Uncovering mechanisms that control immune responses in the resolution of bacterial infections is critical for the development of new therapeutic strategies that resolve infectious inflammation without unwanted side effects. We found that disruption of the vagal system in mice delayed resolution of Escherichia coli infection.  Read more

T-type Ca2+ channels and Autoregulation of Local Blood Flow
Channels
L-type voltage gated Ca2+ channels are considered to be the primary source of calcium influx during the myogenic response. However, many vascular beds also express T-type voltage gated Ca2+ channels. Recent studies suggest that these channels may also play a role in autoregulation.  Read more

Transcriptional and Post-Transcriptional Regulation of Thrombospondin-1 Expression: A Computational Model
PLoS Commputational Biology
Hypoxia is an important physiological stress signal that drives angiogenesis, the formation of new blood vessels. Besides an increase in the production of pro-angiogenic signals such as vascular endothelial growth factor (VEGF), hypoxia also stimulates the production of anti-angiogenic signals. Thrombospondin-1 (TSP-1) is one of the anti-angiogenic factors whose synthesis is driven by hypoxia.  Read more

Thrombospondin-1 Gene Polymorphism Is Associated with Estimated Pulmonary Artery Pressure in Patients with Sickle Cell Anemia
American Journal of Hematology
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Lung vaso-occlusion in sickle cell disease mediated by arteriolar neutrophil-platelet microemboli
Journal of Clinical Investigation Insight
In patients with sickle cell disease (SCD), the polymerization of intraerythrocytic hemoglobin S promotes downstream vaso-occlusive events in the microvasculature. While vaso-occlusion is known to occur in the lung, often in the context of systemic vaso-occlusive crisis and the acute chest syndrome, the pathophysiological mechanisms that incite lung injury are unknown.  Read more

Tumor-Derived Factors and Reduced p53 Promote Endothelial Cell Centrosome Over-Duplication
PLoS One
Approximately 30% of tumor endothelial cells have over-duplicated (>2) centrosomes, which may contribute to abnormal vessel function and drug resistance. Elevated levels of vascular endothelial growth factor A induce excess centrosomes in endothelial cells, but how other features of the tumor environment affect centrosome over-duplication is not known.  Read more