These observations suggest that both wavelength and cell type influence the cell proliferation response to low-intensity laser irradiation.

These results demonstrate that cultured neuropathic bladder SMCs possess and maintain different characteristics than normal SMCs in vitro. The potential clinical implications of using these cells in conjunction with tissue engineering techniques for the promotion of bladder regeneration requires further investigation.

Understanding the pathogenesis of Alzheimer's disease is of widespread interest because it is an increasingly prevalent disorder that is progressive, fatal, and currently untreatable. The dementia of Alzheimer's disease is caused by neuronal cell death. We demonstrate for the first time that blood vessels isolated from the brains of Alzheimer's disease patients can directly kill neurons in vitro. Either direct co-culture of Alzheimer's disease microvessels with neurons or incubation of cultured neurons with conditioned medium from microvessels results in neuronal cell death. In contrast, vessels from elderly nondemented donors are significantly (P<0.001) less lethal and brain vessels from younger donors are not neurotoxic. Neuronal killing by either direct co-culture with Alzheimer's disease microvessels or conditioned medium is dose- and time-dependent. Neuronal death can occur by either apoptotic or necrotic mechanisms. The microvessel factor is neurospecific, killing primary cortical neurons, cerebellar granule neurons, and differentiated PC-12 cells, but not non-neuronal cell types or undifferentiated PC-12 cells. Appearance of the neurotoxic factor is decreased by blocking microvessel protein synthesis with cycloheximide. The neurotoxic factor is soluble and likely a protein, because its activity is heat labile and trypsin sensitive. These findings implicate a novel mechanism of vascular-mediated neuronal cell death in Alzheimer's disease.

CAP37 is a multifunctional protein isolated from human neutrophils with important implications in host defense and inflammation. It is antimicrobial, mediates monocyte chemotaxis, and binds endotoxin. The interaction of neutrophils with endothelial cells is a central feature in inflammation. The object of this study was to determine whether CAP37, a neutrophil-derived protein, could regulate vascular endothelial cell protein kinase C (PKC), an important signaling enzyme. We found that CAP37 stimulated endothelial PKC activity in both a time- and dose-dependent fashion. This stimulation was comparable in magnitude to that evoked by phorbol myristate acetate. A monospecific antiserum against CAP37 inhibited CAP37-induced PKC activity. To establish a structural basis for this activity, overlapping peptides, based on the sequence of native CAP37 were synthesized. Maximum PKC stimulation was evoked by a peptide corresponding to amino acids 95-122 of native CAP37. This domain was distinct from the antibiotic and endotoxin binding domain of the molecule, which resides between amino acids 20 and 44. These data demonstrate that CAP37 can alter endothelial cell PKC and suggest that CAP37 may play a role in neutrophil-endothelial interactions.