Ontology highlight
ABSTRACT: Objective
Congenital deficiency of the principal boundary lubricant in cartilage (i.e., lubricin, encoded by the gene PRG4) increases joint friction and causes progressive joint failure. This study was undertaken to determine whether restoring lubricin expression in a mouse model would prevent, delay, or reverse the disease process caused by congenital deficiency.Methods
Using genetically engineered lubricin-deficient mice, we restored gene function before conception or at ages 3 weeks, 2 months, or 6 months after birth. The effect of restoring gene function (i.e., expression of lubricin) on the tibiofemoral patellar joints of mice was evaluated histologically and by ex vivo biomechanical testing.Results
Restoring gene function in mice prior to conception prevented
SUBMITTER: Hill A
PROVIDER: S-EPMC4626303 | biostudies-literature | 2015 Nov
REPOSITORIES: biostudies-literature