权益分类	功能权益	普通用户	{{item.name}}会员
{{category.name}}	{{benefitItem.name}}

Effects of edema on cadherins in small intestine

水肿对小肠钙粘蛋白的影响

基本信息

批准号：
7632114
负责人：
KAREN S URAY
金额：
$ 8.74万
依托单位：
UNIVERSITY OF TEXAS HLTH SCI CTR HOUSTON
依托单位国家：
美国
项目类别：
财政年份：
2006
资助国家：
美国
起止时间：
2006-07-01 至 2011-06-30
项目状态：
已结题

来源：
https://reporter.nih.gov/project-details/7632114
关键词：
Abdomen Address Adhesions Amino Acid Sequence Area Award Biology C-terminal CDC42 gene Cadherin Domain Cadherins Cell Adhesion Cell Adhesion Molecules Cell Culture Techniques Cell-Cell Adhesion Cells Data Development Edema Ethics Fluid Balance Functional disorder Goals Grant Guanosine Triphosphate Phosphohydrolases Hypertension Intestines Ischemia Mediating Mentors Mesentery Messenger RNA Modeling Molecular Monomeric GTP-Binding Proteins Muscle Contraction Myosin Light Chain Kinase Myosin Light Chains Operative Surgical Procedures Organ Outcome Patients Phosphorylation Proteins Rattus Records Regulation Relative (related person)Research Research Proposals Research Training Role Scientist Signal Transduction Small Intestines Smooth Muscle Smooth Muscle Myocytes Tissues Training Training Activity Trauma Two-Dimensional Gel Electrophoresis Venous Western Blotting Writing design in vivo interest interstitial myosin phosphatase programs symposium

项目摘要

DESCRIPTION (provided by applicant): Interstitial edema, often associated with abdominal surgery or trauma, has been shown to cause intestinal dysfunction including decreased transit. Thus, intestinal edema development has significant negative impact on the outcome of ICU and post-surgical patients. Preliminary data suggests that edema disrupts signaling by the cell-cell adhesion molecule, cadherin. The general hypothesis is that edema induces tissue remodeling that leads to organ dysfunction. The goal is to investigate the effects of edema at the cellular and molecular level in order to understand the mechanism by which edema induces dysfunction. The specific hypothesis to be addressed in this proposal is that edema disrupts cadherin-mediated cell-cell contacts in intestinal smooth muscle causing a decrease in intestinal transit. The first specific aim is designed to examine the effects of intestinal edema on cadherin signaling in vivo using a venous hypertension rat model. The second specific aim is to correlate changes in cadherin signaling with changes in intestinal contractility in the rat intestinal edema model. In the third specifc aim, an intestinal smooth muscle cell culture model will be used to elucidate the role of cadherins in smooth muscle contraction. The fourth specific aim is designed to determine the mechanisms by which edema induces alterations in cadherins. The candidate will gain expertise in a relatively new area of cell adhesion while pursuing her long term research interests in fluid balance and microvascular research. The sponor and co-sponsors are experts in their respective fields and have proven track records in training young scientists. The research proposal and training plan will help the candidate establish an independent and complementary research program within the Microvascular Research Group. The KO1 award will facilitate the candidate's progression to independence by supporting the research training activities while the proposed research is being completed including mentoring by experts in the fields of intestinal function, smooth muscle biology, and cadherin/catenin signaling, attending research conferences relative to her area of research, and taking grant writing and ethics courses.

描述（由申请人提供）：