WOUND HEALING AND EXTRACELLULAR MATRIX REMODELING IN THE LUNGS
WOUND HEALING AND EXTRACELLULAR MATRIX REMODELING IN THE LUNGS
批准号:
8170988
负责人:
Steven CARL George
金额:
$0.18万
依托单位国家:
美国
项目类别:
财政年份:
2010
资助国家:
美国
项目状态:
已结题
起止时间:
2010-08-01 至 2011-07-31
关键词:
AddressAsthmaCellsComputer Retrieval of Information on Scientific Projects DatabaseDiseaseEpithelial CellsExtracellular MatrixFibrosisFundingGrantHyperplasiaIncidenceInjuryInstitutionLungMucous body substancePopulationPrevalenceProcessResearchResearch PersonnelResourcesSeverity of illnessSmooth Muscle MyocytesSourceSymptomsUnited States National Institutes of HealthWound Healingairway remodelingangiogenesisin vitro Modelresponse
中文摘要
这个子项目是许多研究子项目中的一个
由NIH/NCRR资助的中心赠款提供的资源。子项目和
研究者(PI)可能从另一个NIH来源获得了主要资金,
因此可以在其他CRISP条目中表示。所列机构为
研究中心,而研究中心不一定是研究者所在的机构。
支气管哮喘困扰着超过10%的美国人口,并且发病率和患病率都在上升。该疾病的一个关键特征是气道壁的结构变化,其随着疾病进展而变得更加突出,并且与疾病严重程度和症状相关。目前尚不清楚这些变化是否是对异常损伤的正常反应,或者反应本身是否异常。此外,没有足够的信息描述气道重塑的机制,以确定结构变化是否可逆。气道壁的主要变化包括粘液细胞增生、上皮下纤维化、血管生成和平滑肌细胞增生。我们正在开发体外模型来解决所有这些特征,其中心假设是支气管上皮细胞协调和调节这些过程。
英文摘要
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.
Bronchial asthma afflicts more than 10% of the U.S. population, and the incidence and prevalence are on the rise. A critical feature of the disease is structural changes in the wall of the airways, which become more prominent as the disease progresses, and are correlated with disease severity and symptoms. It is not clear whether these changes are a normal response to an abnormal injury, or whether the response itself is abnormal. In addition, there is inadequate information describing the mechanisms of airway remodeling to determine whether the structural changes are reversible. The major changes in the airway wall include mucus cell hyperplasia, subepithelial fibrosis, angiogenesis, and smooth muscle cell hyperplasia. We are developing in vitro models to address all of these features, with a central hypothesis that the bronchial epithelial cell orchestrates and modulates each of these processes.
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