HYALURONAN AND ITS RECEPTORS IN BPD

点击翻译按钮获取中文摘要

This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. The central hypothesis of this proposal is that elevated concentrations of low molecular weight (LMW) Hyaluronan(HA) and post-translational modification of pulmonary collectins, occurring as a result of oxidative, nitrative and nitrosative stresses associated with preterm birth and ventilation, are integral to and promote the inflammatory process that precedes the development of bronchopulmonary dysplasia (BPD). Therapies that limit the production or effects of LMW HA and modified collectins will limit the incidence and/or the severity of BPD. The specific aims proposed were: 1. Characterize the developmental and postnatal expression of HA, its receptors, HA synthases and hyaluronidases in relation to inflammation and markers of oxidation, nitration and nitrosylation in the preterm baboon models of BPD. 2. Characterize the changes in oxidation, nitration and nitrosylation status of pulmonary collectins as a function of gestational age and postnatal interventions after preterm birth. 3. Determine the effects of potential therapies on the inflammatory, HA and its receptors and surfactant changes in the baboon BPD models.