Angiostatin prevents IL-1ß-induced down-regulation of eNOS expression by inhibiting the NF-κB cascade.

This study aimed to elucidate the protective potential of angiostatin in inflamed endothelial cells in culture. We assessed the effect of angiostatin on the expression of ICAM-1 and eNOS. Angiostatin prevented IL-1ß-induced down-regulation of eNOS expression, but produced no significant changes on IL-1ß-induced up-regulation of ICAM-1. We then explored the effect of angiostatin on IL-1ß-mediated inflammatory signaling and found that angiostatin inhibited IL-1ß-mediated nuclear translocation of NF-κB. Thus, our results suggest that angiostatin prevents IL-1ß-induced down-regulation of eNOS expression via inhibition of the NF-κB cascade; this may be the anti-inflammatory mechanism of angiostatin.

Attenuated sensory deprivation-induced changes of parvalbumin neuron density in the barrel cortex of FcγRllB-deficient mice.

Recent studies have demonstrated the important role of immune molecules in the development of neuronal circuitry and synaptic plasticity. We have detected the presence of FcγRllB protein in parvalbumin-containing inhibitory interneurons (PV neurons). In the present study, we examined the appearance of PV neurons in the barrel cortex and the effect of sensory deprivation in FcγRllB-deficient mice (FcγRllB-/-) and wild-type mice. There was no substantial difference in the appearance of PV neurons in the developing barrel cortex between FcγRllB-/- and wild-type mice. Sensory deprivation from immediately after birth (P0) or P7 to P12-P14 induced an increase in PV neurons. In contrast, sensory deprivation from P7 or P14 to P28, but not from P21 to P28, decreased PV neurons in wild-type mice. However, sensory deprivation from P0 or P7 to P12-P14 did not increase PV neurons and sensory deprivation from P7 or P14 to P28 did not decrease or only modestly decreased PV neurons in FcγRllB-/- mice. The results indicate that expression of PV is regulated by sensory experience and the second and third postnatal weeks are a sensitive period for sensory deprivation, and suggest that FcγRllB contributes to sensory experience-regulated expression of PV.