arterial endothelium
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Abstract A simple equation modelling an inextensible elastic lining of an inner-lined tube subject to an imposed pressure difference is derived from a consideration of the idealised elastic properties of the lining and the pressure and soft-substrate forces. Two cases are considered in detail, one with prominent wrinkling and a second one in which wrinkling is absent and only buckling remains. Bifurcation diagrams are computed via numerical continuation for both cases. Wrinkling, buckling, folding, and mixed-mode solutions are found and organised according to system-response measures including tension, in-plane compression, maximum curvature and energy. Approximate wrinkle solutions are constructed using weakly nonlinear theory, in excellent agreement with numerics. Our approach explains how the wavelength of the wrinkles is selected as a function of the parameters in compressed wrinkling systems and shows how localised folds and mixed-mode states form in secondary bifurcations from wrinkled states. Our model aims to capture the wrinkling response of arterial endothelium to blood pressure changes but applies much more broadly.

A 26-year-old man with symptomatic SARS-CoV-2 infection developed a sudden-onset acute testicular pain. The echo-doppler images showed massive testicular infarction, so orchiectomy was performed. On gross examination, the surgical specimen showed complete testicular necrosis and diffuse thickening of the testicular coverings. Under the microscope, a severe obliterative arteritis was evidenced. SARS-CoV-2 spike antibody was detected by immunohistochemistry in the arterial endothelium. Electron microscopy displayed intracytoplasmic spiky viral particles in endothelial cells. The patient was treated with corticoids and was asymptomatic at last contact.

The endothelial cell barrier regulates the passage of fluid between the bloodstream and underlying tissues, and barrier function impairment exacerbates the severity of inflammatory insults. To understand how inflammation alters vessel permeability, we studied the effects of the proinflammatory cytokine TNFα on transendothelial permeability and electrophysiology in ex vivo murine veins and arteries. We found that TNFα specifically decreased the barrier function of venous endothelium without affecting that of arterial endothelium. On the basis of RNA expression profiling and protein analysis, we found that claudin-11 (CLDN11) was the predominant claudin in venous endothelial cells and that there was little, if any, CLDN11 in arterial endothelial cells. Consistent with a difference in claudin composition, TNFα increased the permselectivity of Cl− over Na+ in venous but not arterial endothelium. The vein-specific effects of TNFα also required the activation of Pannexin 1 (Panx1) channels and the CD39-mediated hydrolysis of ATP to adenosine, which subsequently stimulated A2A adenosine receptors. Moreover, the increase in vein permeability required the activation of the Ca2+ channel TRPV4 downstream of Panx1 activation. Panx1-deficient mice resisted the pathologic effects of sepsis induced by cecal ligation and puncture on life span and lung vascular permeability. These data provide a targetable pathway with the potential to promote vein barrier function and prevent the deleterious effects of vascular leak in response to inflammation.

COVID-19 may predispose to both venous and arterial thromboembolic disease due to excessive inflammation, hypoxia, and immobilization. Remarkably, thrombotic complications have hardly been described. We describe a patient with severe pneumonia, COVID-19 correlated, who developed a presumable and rare form of thromboangioiitis with cerebrovascular thrombotic complication and neurological symptoms, in absence of other cardio-vascular risk factor. Significant inflammation is present in our patient, which may explain more dramatic activation of coagulation and arterial endothelium vessels damage. The probable mechanism of this cardiovascular injury may be a direct effect of coronavirus related to Angiotensin-converting enzyme 2 receptor (ACE2-r). The exact mechanisms by which COVID-19 induced hypercoagulability remain incompletely elucidated and more research are necessary.

Adiponectin is the adipokine associated with insulin sensitization, reducing liver gluconeogenesis, and increasing fatty acid oxidation and glucose uptake. Adiponectin is present in the kidneys, mainly in the arterial endothelium and smooth muscle cells, as well as in the capillary endothelium, and might be considered as a marker of many negative factors in chronic kidney disease. The last few years have brought a rising body of evidence that adiponectin is a multipotential protein with anti-inflammatory, metabolic, anti-atherogenic, and reactive oxygen species (ROS) protective actions. Similarly, adiponectin has shown many positive and direct actions in kidney diseases, and among many kidney cells. Data from large cross-sectional and cohort studies showed a positive correlation between serum adiponectin and mortality in chronic kidney disease. This suggests a complex interaction between local adiponectin action, comorbidities, and uremic milieu. In this review we discuss the role of adiponectin in chronic kidney disease.