<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Kusewitt DF</submitter><funding>NCI NIH HHS</funding><funding>National Institutes of Health</funding><funding>NIGMS NIH HHS</funding><pagination>106607</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC11444091</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>244</volume><pubmed_abstract>Long-term administration of exogenous estrogen is known to cause urinary retention and marked, often fatal, bladder distention in both male and female mice. Estrogen-treated mice have increased bladder pressure and decreased urine flow, suggesting that urinary retention in estrogen-treated mice is due to infravesicular obstruction to urine outflow. Thus, the condition is commonly referred to as bladder outlet obstruction (BOO). Obesity can also lead to urinary retention. As the effects of estrogen are mediated by multiple receptors, including estrogen receptors ERα and ERβ and the G protein-coupled estrogen receptor (GPER), we sought to determine whether GPER plays a role in estrogen-induced BOO, particularly in the context of obesity. Wild type and GPER knockout (KO) mice fed a high-fat d</pubmed_abstract><journal>The Journal of steroid biochemistry and molecular biology</journal><pubmed_title>GPER expression prevents estrogen-induced urinary retention in obese mice.</pubmed_title><pmcid>PMC11444091</pmcid><funding_grant_id>P30 CA016058</funding_grant_id><funding_grant_id>R01 CA194496</funding_grant_id><funding_grant_id>P20 GM121176</funding_grant_id><funding_grant_id>K12 GM088021</funding_grant_id><funding_grant_id>R01 CA163890</funding_grant_id><funding_grant_id>P30 CA118100</funding_grant_id><pubmed_authors>Woods CD</pubmed_authors><pubmed_authors>Prossnitz ER</pubmed_authors><pubmed_authors>Rosas E</pubmed_authors><pubmed_authors>Sharma G</pubmed_authors><pubmed_authors>Hathaway HJ</pubmed_authors><pubmed_authors>Kusewitt DF</pubmed_authors></additional><is_claimable>false</is_claimable><name>GPER expression prevents estrogen-induced urinary retention in obese mice.</name><description>Long-term administration of exogenous estrogen is known to cause urinary retention and marked, often fatal, bladder distention in both male and female mice. Estrogen-treated mice have increased bladder pressure and decreased urine flow, suggesting that urinary retention in estrogen-treated mice is due to infravesicular obstruction to urine outflow. Thus, the condition is commonly referred to as bladder outlet obstruction (BOO). Obesity can also lead to urinary retention. As the effects of estrogen are mediated by multiple receptors, including estrogen receptors ERα and ERβ and the G protein-coupled estrogen receptor (GPER), we sought to determine whether GPER plays a role in estrogen-induced BOO, particularly in the context of obesity. Wild type and GPER knockout (KO) mice fed a high-fat d</description><dates><release>2024-01-01T00:00:00Z</release><publication>2024 Nov</publication><modification>2026-06-05T07:32:28.758Z</modification><creation>2026-05-14T03:12:55.231Z</creation></dates><accession>S-EPMC11444091</accession><cross_references><pubmed>39197539</pubmed><doi>10.1016/j.jsbmb.2024.106607</doi></cross_references></HashMap>