microRNA 在肾脏钠调节中的作用-猫眼课题宝

microRNA 在肾脏钠调节中的作用

批准号：

9054837

负责人：

Michael B Butterworth

金额：

$34.65万

依托单位：

UNIVERSITY OF PITTSBURGH AT PITTSBURGH

依托单位国家：

美国

项目类别：

财政年份：

2015

资助国家：

美国

项目状态：

已结题

起止时间：

2015-05-01 至 2020-04-30

来源：

https://reporter.nih.gov/project-details/9054837

关键词：

Address Adrenal Cortex Hormones Aldosterone Angiotensin II Area CYP11B2 gene Cells Collaborations Collecting Cell Cortical Nephron Development Diet Disease Distal Duct (organ) structure Electrolytes Epithelial Epithelium Equilibrium Family Future Genomics Health Homeostasis Hormonal Hormones Hypertension Hypoaldosteronism Hypotension Intervention Kidney Kidney Diseases Knock-out Knockout Mice Link Mediating Mediator of activation protein MicroRNAs Mineralocorticoid Receptor Mineralocorticoids Modeling Nephrons Pathway interactions Phosphorylation Physiology Positioning Attribute Potassium Proteins Recycling Regulation Regulatory Pathway Reporting Role Scaffolding Protein Signal Pathway Signal Transduction Sodium Sodium Channel Sodium Chloride Syndrome Testing Transgenic Organisms Untranslated RNA Work epithelial Na+ channel human disease in vivo intersectin 1 mouse model novel response trafficking uptake

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英文摘要

DESCRIPTION (provided by applicant): This proposal will investigate the role of small non-coding RNAs, termed microRNAs (miRs), in the regulation of sodium (Na+) transport in the distal kidney nephron. We will investigate the hypothesis that the mineralocorticoid hormone, aldosterone regulates the expression of specific miR clusters in the distal kidney nephron cortical collecting duct (CCD), to alter Na+ transport by targeting the expression of the scaffold protein intersectin-2. Using in vivo mouse models we will establish the regulation of miRs in the principal cells of the CCD. The significantly regulated miRs that are altered by aldosterone and other signaling pathways linked to sodium regulation will be determined. We will alter the expression of the miR-23~24~27 clusters to demonstrate its importance in maintaining sodium balance in the kidney. Finally the mechanism of intersectin-2 regulation of the epithelial sodium channel will be determined, to characterize the involvement of this novel aldosterone-repressed protein in Na+ regulation in the kidney.

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