2008 Grover Conference on Pulmonary Vascular Pathobiology

描述(由申请人提供)： 本申请申请资助2008年格罗弗肺循环会议，题为“肺循环中的膜受体、通道和转运体：在肺血管疾病发展中的作用”。 受体、通道和转运体在信号转导中起关键作用，是肺血管疾病(PVD)发生发展的关键因素。它们代表了调节成纤维细胞、平滑肌和内皮细胞动态平衡的前线机制，以及对细胞外环境和细胞间介质的反应。膜受体和离子通道功能和表达的紊乱导致细胞功能的深刻变化，并在PVD的发生和发展中起重要作用。 在过去的十年里，我们对新型膜受体、通道和转运体在肺循环中的表达和功能的了解取得了重大进展。一些新的分子类离子通道(如色氨酸和双孔结构域K+通道)在肺血管功能中起关键作用。先进的分子技术、基因敲除模型和人类基因组计划为离子K+和氯通道、水通道和细胞内钙通道在肺血管功能和疾病中的分子识别和作用提供了进一步的见解。疾病发展与骨形态发生蛋白受体II(BMPRII)突变之间的关联代表了该领域的一项重大进展。BMPR、5-羟色胺受体和转运体以及离子通道之间存在显著的相互作用；这种相互关系很可能决定了肺血管疾病中收缩和重构改变的很大比例。我们认为需要一个论坛，在那里可以讨论这些机制和途径，以揭示潜在的融合治疗机会。 2008年Grover会议为肺血管病理生物学和肺血管疾病临床管理领域的专家提供了一个论坛，以严格讨论1)膜受体、通道和转运体及其在肺血管功能调节中的作用的最新进展；2)与肺血管疾病发病机制有关的相互关系；3)可能存在的治疗机会。(摘要结束)

DESCRIPTION (provided by applicant): This application requests funding to support the 2008 Grover Conference on the Pulmonary Circulation, entitled "Membrane Receptors, Channels and Transporters in the Pulmonary Circulation: Role in the Development of Pulmonary Vascular Disease." Receptors, channels and transporters play critical roles in signal transduction, and are key elements in the development and progression of pulmonary vascular disease (PVD) progression. They represent the frontline mechanisms regulating fibroblast, smooth muscle and endothelial cell homeostasis, and for responding to the extracellular environment and intercellular mediators. Perturbations in membrane receptor and ion channel function and expression cause profound alterations in cellular function and significantly contribute to pathogenesis and progression of PVD. Over the past decade, there have been significant advances in our understanding of the expression and function of novel membrane receptors, channels and transporters in the pulmonary circulation. Several new molecular classes of ion channels (e.g., TRP and two-pore domain K+ channels) have been shown to play key roles in pulmonary vascular function. Enhanced molecular techniques, gene knockout models, and the human genome project have provided further insight into the molecular identity and role of ion K+ and Cl channels, aquaporins and intracellular Ca2+ channels in pulmonary vascular function and disease. The association between disease development and bone morphogenetic protein receptor II (BMPRII) mutations represents a major advance in the field. There are significant interactions between BMPR, serotonin receptors and transporters, and ion channels; such interrelationships will likely define a significant proportion of the altered contractility and remodeling in pulmonary vascular disease. We see a need for a forum where these mechanisms and pathways can be discussed to reveal potential converging therapeutic opportunities. The 2008 Grover Conference provides a forum for experts in the fields of pulmonary vascular pathobiology and clinical management of pulmonary vascular disease to rigorously address 1) recent advances in our knowledge of membrane receptors, channels and transporters and their role in regulation of pulmonary vascular function; 2) the interrelationships that contribute to the pathogenesis of pulmonary vascular disease, and 3) the therapeutic opportunities that may exist. (End of Abstract)