Wnt7a Decreases Brain Endothelial Barrier Function Via β-Catenin Activation.

The blood-brain barrier consists of tightly connected endothelial cells protecting the brain's microenvironment from the periphery. These endothelial cells are characterized by specific tight junction proteins such as Claudin-5 and Occludin, forming the endothelial barrier. Disrupting these cells might lead to blood-brain barrier dysfunction.

Interventions in WNT Signaling to Induce Cardiomyocyte Proliferation: Crosstalk with Other Pathways.

Myocardial infarction is a frequent cardiovascular event and a major cause for cardiomyocyte loss. In adult mammals, cardiomyocytes are traditionally considered to be terminally differentiated cells, unable to proliferate. Therefore, the wound-healing response in the infarct area typically yields scar tissue rather than newly formed cardiomyocytes.

Wnt Signaling in Cardiac Remodeling and Heart Failure.

Wnt signaling plays an essential role during development, but is also activated in diseases as diverse as neurodegeneration, osteoporosis, and cancer. Accumulating evidence demonstrates that Wnt signaling is also activated during cardiac remodeling and heart failure. In this chapter, we will provide a brief overview of Wnt signaling in all its complexity.

Diurnal rhythms of serum and plasma cytokine profiles in healthy elderly individuals assessed using membrane based multiplexed immunoassay.

Background: Recent clinical studies suggest that inflammatory mediators have huge potential in individualized therapy and in efficacy screening and can be utilized as biomarkers for a plethora of pathological conditions. The standard approach for detecting and measuring these inflammatory mediators is via blood samples. Nevertheless, there is no scientific report providing solid evidence on the most suitable blood compartment that will give the optimal inflammatory mediator measurement, or regarding the diurnal variation of circulating mediators.

Cardiac (myo)fibroblast: Novel strategies for its targeting following myocardial infarction.

Following myocardial infarction (MI), a dynamic and complex process called wound healing is initiated, aiming to produce a robust scar and limit adverse remodeling of the left ventricle (LV). Cardiac fibroblasts (CFs) - the most populous cardiac cell-type - differentiate into myofibroblasts under the influence of post-MI mechanical stress, transforming growth factor β (TGF-β) and various inflammatory signals. Myofibroblasts are contractile cells that start producing extracellular matrix (ECM) components and secrete factors that orchestrate wound healing, but also promote adverse cardiac remodeling that can progress to life-threatening heart failure (HF).

Interventions in Wnt signaling as a novel therapeutic approach to improve myocardial infarct healing.

Following myocardial infarction, wound healing takes place in the infarct area where the non-viable cardiac tissue is replaced by a scar. Inadequate wound healing or insufficient maintenance of the extracellular matrix in the scar can lead to excessive dilatation of the ventricles, one of the hallmarks of congestive heart failure. Therefore, it is important to better understand the wound-healing process in the heart and to develop new therapeutic agents that target the infarct area in order to maintain an adequate cardiac function.