Id Proteins Regulate Capillary Repair and Perivascular Cell Proliferation following Ischemia-Reperfusion Injury

摘要: Acute kidney injury (AKI) results in microvascular damage that if not normally repaired, may lead to fibrosis. The Id1 and 3 proteins have a critical role promoting angiogenesis during development, tumor growth wound repair by functioning as dominant negative regulators of bHLH transcription factors. goal this study was determine Id regulate remodeling increased expression decreased capillary loss following AKI. effect changes vivo examined using Id1−/−, Id3RFP/+ (Id1/Id3 KO) Tek (Tie2)-rtTA, TRE-lacz/TRE (TRE Id1) mice with doxycycline inducible endothelial β-galactosidase expression. were co-localized cells normal adult kidneys protein levels at day ischemia-reperfusion (IRI) contralateral nephrectomy. Id1/Id3 KO had baseline density pericyte coverage tubular IRI but interstitial cell proliferation fibrosis compared WT littermates. No compensatory increase size occurred resulting creatinine TRE mice. no rarefaction within 1 week comparison PDGFRβ positive medullary collagen deposition developed albuminuria later time points. These differences associated Angiopoietin (Ang1) Ang2 Examination gene isolated from WT, showed Ang1 αSMA overexpressing markers suggest AKI result