PDGF-BB regulates splitting angiogenesis in skeletal muscle by limiting VEGF-induced endothelial proliferation.

VEGF induces normal or aberrant angiogenesis depending on its dose in the microenvironment around each producing cell in vivo. This transition depends on the balance between VEGF-induced endothelial stimulation and PDGF-BB-mediated pericyte recruitment, and co-expression of PDGF-BB normalizes aberrant angiogenesis despite high VEGF doses. We recently found that VEGF over-expression induces angiogenesis in skeletal muscle through an initial circumferential vascular enlargement followed by longitudinal splitting, rather than sprouting.

Procalcitonin Impairs Endothelial Cell Function and Viability.

Background: Procalcitonin is used as a diagnostic tool for the identification and risk stratification of septic patients. Procalcitonin plasma concentrations tightly correlate with the severity of the ongoing inflammatory reaction and can rise up to 10,000-fold. Impairment of endothelial cell function plays an important role in the pathogenesis of hypotension and disturbed organ perfusion during sepsis.

New TiAg composite coating for bone prosthesis engineering shows promising microvascular compatibility in the murine dorsal skinfold chamber model.

The incorporation of antimicrobial substances like silver into implant surface coatings is one promising concept against primary infections of endoprosthesis, especially for immunocompromised patients as well as against reinfection after revision operations. However, besides good antimicrobial and mechanical properties it is equally important that the implant material does not disturb the local microvascular perfusion of muscle tissue to enable microbial host defense and tissue repair processes. In this study the biocompatibility of a newly developed TiAg-composite coating applied on conventional titanium via physical vapor deposition was analysed.

Protein z exerts pro-angiogenic effects and upregulates CXCR4.

Objective: Protein Z (PZ) is a vitamin K-dependent coagulation factor without catalytic activity. Evidence points towards PZ as an independent risk factor for the occurrence of human peripheral arterial disease. However, the role of PZ in ischemia-driven angiogenesis and vascular healing processes has not been elucidated so far.

Protein Z-deficiency is associated with enhanced neointima formation and inflammatory response after vascular injury in mice.

Background: Protein Z (PZ) is a vitamin K-dependent coagulation factor without catalytic activity. Evidence points towards PZ as an independent risk factor for the occurrence of human atherosclerotic vascular diseases. The aim of this study was to investigate the role of PZ in vascular arterial disease.