Potent lentiviral restriction by a synthetic feline TRIM5 cyclophilin A fusion.

A synthetic feline TRIM5-cyclophilin A fusion protein (feTRIMCyp) was generated and transduced into feline cells. feTRIMCyp was highly efficient at preventing infection with human (HIV) and feline (FIV) immunodeficiency virus pseudotypes, and feTRIMCyp-expressing cells resisted productive infection with either FIV-Fca or FIV-Pco. The restriction of FIV infection by feTRIMCyp was reversed by the cyclosporine (Cs) derivatives NIM811 and Debio-025 but less so by Cs itself.

The mouse aorta model: influence of genetic background and aging on bFGF- and VEGF-induced angiogenic sprouting.

Angiogenesis can be studied ex vivo by culturing rat or mouse aortic rings in collagen gels. Unlike rat aorta explants, unstimulated mouse aortic rings were unable to spontaneously produce an angiogenic response under serum-free conditions. They, however, responded to bFGF and VEGF, generating networks of branching neovessels.

Chlamydia pneumoniae induces Alzheimer-like amyloid plaques in brains of BALB/c mice.

Amyloid deposits resembling plaques found in Alzheimer's disease (AD) brains were formed in the brains of non-transgenic BALB/c mice following intranasal infection with Chlamydia pneumoniae. The mice were infected at 3 months of age with C. pneumoniae isolated from an AD brain.

Chlamydia pneumoniae infection alters the junctional complex proteins of human brain microvascular endothelial cells.

Chlamydia pneumoniae has been identified and associated with multiple sclerosis (MS) and Alzheimer's disease (AD) pathogenesis, although the relationship of this organism in these diseases remains controversial. We have hypothesized that one potential avenue of infection is through the junctional complexes between the blood-brain barrier (BBB) endothelia. C.

Regulation of angiogenesis by vascular endothelial growth factor and angiopoietin-1 in the rat aorta model: distinct temporal patterns of intracellular signaling correlate with induction of angiogenic sprouting.

Vascular endothelial growth factor (VEGF) and angiopoietin-1 (Ang-1) promote the spontaneous angiogenic response of freshly cut rat aortic rings. When VEGF and Ang-1 were tested in cultures of 14-day-old rings, which are quiescent and unable to spontaneously produce neovessels, only VEGF was capable of inducing an angiogenic response. Ang-1 failed to initiate angiogenesis in this system, but significantly potentiated VEGF-induced neovessel sprouting.