Karin Aase

TL;DR: A new PDGF, PDGF-C, is identified, which binds to and activates the PDGF α-receptor and is activated by proteolysis and induces proliferation of fibroblasts when overexpressed in transgenic mice.

TL;DR: The binding of VEGF-B to its receptor on endothelial cells leads to increased expression and activity of urokinase type plasminogen activator and plasmineg activator inhibitor 1, suggesting a role for VEGf-B in the regulation of extracellular matrix degradation, cell adhesion, and migration.

TL;DR: The expression of VEGF-C is associated with the development of lymphatic vessels, and VEGf-C could be an important factor regulating the mutual paracrine relationships between tumor cells and lymphatic endothelial cells.

TL;DR: VEGF-B seems to be required for normal heart function in adult animals but is not required for proper development of the cardiovascular system either during development or for angiogenesis in adults.

TL;DR: A transgenic mouse that exhibits cardiac fibrosis followed by hypertrophy with sex-dependent phenotypes is created and reveals that a potent mitogen for cardiac fibroblasts result in an expansion of the interstitium that induce a secondary sex- dependent hypertrophic response in the cardiomyocytes.