Aortic Stiffness in L-NAME Treated C57Bl/6 Mice Displays a Shift From Early Endothelial Dysfunction to Late-Term Vascular Smooth Muscle Cell Dysfunction.

Endothelial dysfunction is recognized as a cardiovascular aging hallmark. Administration of nitric oxide synthase blocker N-Ω-Nitro-L-arginine methyl ester hydrochloride (L-NAME) constitutes a well-known small animal model of cardiovascular aging. Despite extensive phenotypic characterization, the exact aortic function changes in L-NAME treated mice are largely unknown.

Progressive aortic stiffness in aging C57Bl/6 mice displays altered contractile behaviour and extracellular matrix changes.

Aortic stiffness is a hallmark of cardiovascular disease, but its pathophysiology remains incompletely understood. This study presents an in-dept characterization of aortic aging in male C57Bl/6 mice (2-24 months). Cardiovascular measurements include echocardiography, blood pressure measurement, and ex vivo organ chamber experiments.

Mouse aortic biomechanics are affected by short-term defective autophagy in vascular smooth muscle cells.

The physiology of vascular smooth muscle (VSMC) cells is affected by autophagy, a catabolic cellular mechanism responsible for nutrient recycling. Autophagy-inducing compounds may reverse arterial stiffening, whereas congenital VSMC-specific autophagy deficiency promotes arterial stiffening. The elevated aortic stiffness in 3.

Performance of the FREND™ COVID-19 IgG/IgM Duo point-of-care test for SARS-CoV-2 antibody detection.

Purpose: In the context of the current COVID-19 pandemic, multiple serological assays for the detection of severe acute respiratory syndrome 2 (SARS-CoV-2) immune response are currently being developed. This study compares the FREND COVID-19 IgG/IgM Duo (NanoEntec) a point of care (POCT) assay with the automated Elecsys anti-SARS-CoV-2 electrochemiluminescent assay (Roche Diagnostics).

Methods: Serum samples ( = 81) from PCR-confirmed SARS-CoV-2 positive patients at different time points after the onset of symptoms were analyzed with both assays.

GSK-7975A, an inhibitor of Ca release-activated calcium channels, depresses isometric contraction of mouse aorta.

GSK-7975A is described to inhibit stromal interaction molecule 1(STIM1)-mediated Ca release-activated Ca channels ORAI 1, ORAI 2 and ORAI 3 in different cell types. The present study investigated whether isometric contractions of mouse aortic segments were affected by this selective store-operated calcium channel inhibitor. Depending on the way by which Ca influx pathways were activated during contraction, GSK-7975A inhibited contractility of mouse aortic segments with different affinity.

Prdm16 Supports Arterial Flow Recovery by Maintaining Endothelial Function.

[Figure: see text].

Defective Autophagy in Vascular Smooth Muscle Cells Alters Vascular Reactivity of the Mouse Femoral Artery.

Autophagy is an important cellular survival process that enables degradation and recycling of defective organelles and proteins to maintain cellular homeostasis. Hence, defective autophagy plays a role in many age-associated diseases, such as atherosclerosis, arterial stiffening and hypertension. Recently, we showed in mice that autophagy in vascular smooth muscle cells (VSMCs) of large elastic arteries such as the aorta is important for Ca mobilization and vascular reactivity.

Defective autophagy in vascular smooth muscle cells increases passive stiffness of the mouse aortic vessel wall.

Aging and associated progressive arterial stiffening are both important predictors for the development of cardiovascular diseases. Recent evidence showed that autophagy, a catabolic cellular mechanism responsible for nutrient recycling, plays a major role in the physiology of vascular cells such as endothelial cells and vascular smooth muscle cells (VSMCs). Moreover, several autophagy inducing compounds are effective in treating arterial stiffness.

Autophagy as an emerging therapeutic target for age-related vascular pathologies.

: The incidence of age-related vascular diseases such as arterial stiffness, hypertension and atherosclerosis, is rising dramatically and is substantially impacting healthcare systems. Mounting evidence suggests that there is an important role for autophagy in maintaining (cardio)vascular health. Impaired vascular autophagy has been linked to arterial aging and the initiation of vascular disease.

Defective autophagy in vascular smooth muscle cells alters contractility and Ca²⁺ homeostasis in mice.

Autophagy is an evolutionary preserved process that prevents the accumulation of unwanted cytosolic material through the formation of autophagosomes. Although autophagy has been extensively studied to understand its function in normal physiology, the role of vascular smooth muscle (SM) cell (VSMC) autophagy in Ca(2+) mobilization and contraction remains poorly understood. Recent evidence shows that autophagy is involved in controlling contractile function and Ca(2+) homeostasis in certain cell types.