Highlights d VE-cadherin regulates mechanotransduction signaling in the lymphatic vasculature d Loss of VE-cadherin impairs lymphatic valve formation and maintenance d VE-cadherin stabilizes b-catenin to enable regulation of PROX1 and FOXC2 d AKT signaling regulates FOXC2 and is impaired in the absence of VE-cadherin

No abstract

Endothelial cells of the microcirculation form a semi-permeable diffusion barrier between the blood and tissues. This permeability of the endothelium, particularly in the capillaries and postcapillary venules, is a normal physiological function needed for blood-tissue exchange in the microcirculation. During inflammation, microvascular permeability increases dramatically and can lead to tissue edema, which in turn can lead to dysfunction of tissues and organs. The molecular mechanisms that control the barrier function of endothelial cells have been under investigation for several decades, and remain an important topic due to the potential for discovery of novel therapeutic strategies to reduce edema. This review highlights current knowledge of the cellular and molecular mechanisms that lead to endothelial hyperpermeability during inflammatory conditions associated with injury and disease. This includes a discussion of recent findings demonstrating temporal protrusions by endothelial cells that may contribute to intercellular junction integrity between endothelial cells and affect the diffusion distance for solutes via the paracellular pathway.

No abstract

The σ1 is a single 25-kDa transmembrane protein residing primarily in the ER that acts as a chaperone protein. Its interaction with mitochondria at the mitochondria-associated ER membrane domain is well documented. 1 Following activation, σ1 has been reported to bind to the IP 3 R, and modulate intracellular calcium homeostasis. 2 Also, the activated σ1 modulates plasma membrane receptors and ion channel functions, and may regulate cellular excitability. 3-6 Further, σ1 affects trafficking of lipids