<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Huang L</submitter><funding>BLRD VA</funding><funding>NIDDK NIH HHS</funding><funding>NCI NIH HHS</funding><pagination>2303-15</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC4178431</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>25(10)</volume><pubmed_abstract>Stanniocalcin-1 is an intracrine protein; it binds to the cell surface, is internalized to the mitochondria, and diminishes superoxide generation through induction of uncoupling proteins. In vitro, stanniocalcin-1 inhibits macrophages and preserves endothelial barrier function, and transgenic overexpression of stanniocalcin-1 in mice protects against ischemia-reperfusion kidney injury. We sought to determine the kidney phenotype after kidney endothelium-specific expression of stanniocalcin-1 small hairpin RNA (shRNA). We generated transgenic mice that express stanniocalcin-1 shRNA or scrambled shRNA upon removal of a floxed reporter (phosphoglycerate kinase-driven enhanced green fluorescent protein) and used ultrasound microbubbles to deliver tyrosine kinase receptor-2 promoter-driven Cre </pubmed_abstract><journal>Journal of the American Society of Nephrology : JASN</journal><pubmed_title>AKI after conditional and kidney-specific knockdown of stanniocalcin-1.</pubmed_title><pmcid>PMC4178431</pmcid><funding_grant_id>R01 CA116097</funding_grant_id><funding_grant_id>R01-DK080306</funding_grant_id><funding_grant_id>P30-CA125123</funding_grant_id><funding_grant_id>T32-DK062706</funding_grant_id><funding_grant_id>T32 DK062706</funding_grant_id><funding_grant_id>R01 DK080306</funding_grant_id><funding_grant_id>I01 BX002006</funding_grant_id><funding_grant_id>P30 CA125123</funding_grant_id><funding_grant_id>R01 CA122623</funding_grant_id><pubmed_authors>Belousova T</pubmed_authors><pubmed_authors>Ju H</pubmed_authors><pubmed_authors>Pan JS</pubmed_authors><pubmed_authors>Lu L</pubmed_authors><pubmed_authors>Nuotio-Antar A</pubmed_authors><pubmed_authors>Huang L</pubmed_authors><pubmed_authors>Du J</pubmed_authors><pubmed_authors>Sheikh-Hamad D</pubmed_authors><pubmed_authors>Truong LD</pubmed_authors><pubmed_authors>Zhang P</pubmed_authors></additional><is_claimable>false</is_claimable><name>AKI after conditional and kidney-specific knockdown of stanniocalcin-1.</name><description>Stanniocalcin-1 is an intracrine protein; it binds to the cell surface, is internalized to the mitochondria, and diminishes superoxide generation through induction of uncoupling proteins. In vitro, stanniocalcin-1 inhibits macrophages and preserves endothelial barrier function, and transgenic overexpression of stanniocalcin-1 in mice protects against ischemia-reperfusion kidney injury. We sought to determine the kidney phenotype after kidney endothelium-specific expression of stanniocalcin-1 small hairpin RNA (shRNA). We generated transgenic mice that express stanniocalcin-1 shRNA or scrambled shRNA upon removal of a floxed reporter (phosphoglycerate kinase-driven enhanced green fluorescent protein) and used ultrasound microbubbles to deliver tyrosine kinase receptor-2 promoter-driven Cre </description><dates><release>2014-01-01T00:00:00Z</release><publication>2014 Oct</publication><modification>2026-05-02T00:16:04.947Z</modification><creation>2019-03-27T01:36:40Z</creation></dates><accession>S-EPMC4178431</accession><cross_references><pubmed>24700878</pubmed><doi>10.1681/ASN.2013070690</doi><doi>10.1681/asn.2013070690</doi></cross_references></HashMap>