Cellular mechanisms of toll-like receptor-3 activation in the thalamus are associated with white matter injury in the developing brain.

摘要: Toll-like receptor-3 (TLR3) has been identified in a variety of intracellular structures (e.g. endosomes and endoplasmic reticulum); it detects viral molecular patterns damage-associated patterns. We hypothesized that, after white matter injury (WMI) occurred, localization activation TLR3 are altered gray response to activated glia. Therefore, we investigated the subcellular its downstream signaling pathway postmortem brain sections from preterm infants with without WMI (7 patients each). assessed astroglia (glial fibrillary acidic protein–positive), microglia (ionized calcium-binding adaptor molecule-1–positive), neuronal populations 3 regions thalamus posterior limb internal capsule analyzed messenger RNA protein expression ventral lateral thalamic region, an area associated impaired motor function. also colocalization late (lysosome-associated membrane protein-1) phagosomal compartments this region. Glial protein, ionized molecule-1, immunoreactivity were increased cases compared controls. In neurons, was colocalized reticulum autophagosome, suggesting that autophagy may be stress WMI. Thus, alterations underlying mechanism development infants.