Diabetes causes NLRP3-dependent barrier dysfunction in mice with detrusor overactivity but not underactivity
Michael R. Odom, Francis M. Hughes, Huixia Jin, J. Todd Purves
Abstract
This is the first study to demonstrate that NLRP3-mediated inflammation is responsible for urothelial barrier damage in type 1 diabetic female Akita mice with an overactive bladder. Eliminating the NLRP3 gene in these diabetic mice prevented barrier damage as a result of diabetes. By the time female Akita mice develop an underactive phenotype, the urothelial barrier has been restored, suggesting that inflammation is a critical causative factor early in the development of diabetic bladder dysfunction.
Topics & Concepts
Ex vivoProinflammatory cytokineBarrier functionInflammasomeOccludinInflammationDownregulation and upregulationIn vivoEvans BluePyroptosisNodPyrin domainChemistryTight junctionEndocrinologyMedicineDiabetes mellitusCell biologyInternal medicineBiologyBiochemistryBiotechnologyGeneUrinary Bladder and Prostate ResearchPelvic floor disorders treatmentsUrinary Tract Infections Management