Endothelial cell promotion of early liver and pancreas development.

Different steps of embryonic pancreas and liver development require inductive signals from endothelial cells. During liver development, interactions between newly specified hepatic endoderm cells and nascent endothelial cells are crucial for the endoderm's subsequent growth and morphogenesis into a liver bud. Reconstitution of endothelial cell stimulation of hepatic cell growth with embryonic tissue explants demonstrated that endothelial signalling occurs independent of the blood supply.

Fetal tracheal reconstruction with cartilaginous grafts engineered from mesenchymal amniocytes.

Background/purpose: This study was aimed at determining whether cartilaginous grafts engineered from mesenchymal cells normally present in the amniotic fluid could be used in fetal tracheal repair.

Methods: Ovine mesenchymal amniocytes were expanded in culture, labeled with green fluorescent protein, and seeded onto biodegradable scaffold tubes maintained in chondrogenic medium. After chondrogenic differentiation of the constructs was confirmed, they were used to repair either partial or full circumferential tracheal defects in allogeneic fetal lambs (n = 7).

An injectable tissue-engineered embolus prevents luminal recanalization after vascular sclerotherapy.

Background/purpose: Sclerotherapy for vascular malformations is often limited by luminal recanalization. This study examined whether an injectable tissue-engineered construct could prevent this complication in a rabbit model of venous sclerotherapy.

Methods: Ethanol sclerotherapy of a temporarily occluded jugular vein segment was performed in 46 rabbits, which were then divided into 3 groups.

CDK2 translational down-regulation during endothelial senescence.

Here we report for the first time that loss of CDK2 activity, by translational inhibition and through CDK2 inhibition by p21(Cip1/Waf1), may be responsible for endothelial senescence. We show that expression of dominant-negative p53 extends human umbilical vein endothelial cell (HUVEC) lifespan past senescence. HUVEC expressing telomerase can completely bypass senescence and become immortal (i-HUVEC).

Enhancement of intravascular sclerotherapy by tissue engineering: short-term results.

Background/purpose: Treatment of vascular malformations with sclerotherapy is often complicated by reexpansion secondary to endothelial recanalization. This study examined the use of an autologous fibroblast construct to enhance intraluminal scar formation after sclerotherapy.

Methods: New Zealand rabbits (n = 15) underwent ethanol sclerotherapy of a segment of the facial vein.

Senescence and its bypass in the vascular endothelium.

Vascular endothelial cells line the interior of blood vessels. As in other cell types, the proliferative lifespan of endothelial cells is limited; after a given number of replication cycles, they undergo senescence. Angiogenesis, the formation of new capillaries from pre-existing vasculature, is a process that involves endothelial cell proliferation.

Maintenance of G1 checkpoint controls in telomerase-immortalized endothelial cells.

Here we report the characterization of a series of telomerase-immortalized human umbilical vein endothelial cell lines (i-HUVEC). These cells maintain endothelial characteristics such as marker expression, dependence on basic fibroblast growth factor for proliferation, and the ability to form tube structures on Matrigel. In addition, these cells do not show signs of tumorigenic transformation because their growth is contact-inhibited, serum-dependent, and anchorage-dependent.

Binding inhibition of angiogenic factors by heparan sulfate proteoglycans in aqueous humor: potential mechanism for maintenance of an avascular environment.

Aqueous humor is a clear fluid, primarily a blood filtrate, which circulates through the anterior chamber of the eye and bathes the cornea. We explored the possibility that components in the aqueous humor play a direct part in maintaining the avascular environment of the cornea. We report here that heparan sulfate proteoglycan (HSPG) was found in bovine aqueous humor and that it directly inhibits binding of basic fibroblast growth factor and vascular endothelial growth factor to cell-surface heparan sulfate.

PPARgamma ligands inhibit primary tumor growth and metastasis by inhibiting angiogenesis.

Several drugs approved for a variety of indications have been shown to exhibit antiangiogenic effects. Our study focuses on the PPARgamma ligand rosiglitazone, a compound widely used in the treatment of type 2 diabetes. We demonstrate, for the first time to our knowledge, that PPARgamma is highly expressed in tumor endothelium and is activated by rosiglitazone in cultured endothelial cells.