{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Kuo IY"],"funding":["NIDDK NIH HHS","NIH HHS"],"pagination":["e0153632"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC4833351"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["11(4)"],"pubmed_abstract":["Mutations in the gene for polycystin 2 (Pkd2) lead to polycystic kidney disease, however the main cause of mortality in humans is cardiac related. We previously showed that 5 month old Pkd2+/- mice have altered calcium-contractile activity in cardiomyocytes, but have preserved cardiac function. Here, we examined 1 and 9 month old Pkd2+/- mice to determine if decreased amounts of functional polycystin 2 leads to impaired cardiac function with aging. We observed changes in calcium handling proteins in 1 month old Pkd2+/- mice, and these changes were exacerbated in 9 month old Pkd2+/- mice. Anatomically, the 9 month old Pkd2+/- mice had thinner left ventricular walls, consistent with dilated cardiomyopathy, and the left ventricular ejection fraction was decreased. Intriguingly, in response to acute isoproterenol stimulation to examine ?-adrenergic responses, the 9 month old Pkd2+/- mice exhibited a stronger contractile response, which also coincided with preserved localization of the ?2 adrenergic receptor. Importantly, the Pkd2+/- mice did not have any renal impairment. We conclude that the cardiac-related impact of decreased polycystin 2 progresses over time towards cardiac dysfunction and altered adrenergic signaling. These results provide further evidence that polycystin 2 provides a critical function in the heart, independent of renal involvement."],"journal":["PloS one"],"pubmed_title":["Decreased Polycystin 2 Levels Result in Non-Renal Cardiac Dysfunction with Aging."],"pmcid":["PMC4833351"],"funding_grant_id":["5P30DK034989","K99DK101585","S10 OD020142","OD020142","P01 DK057751","P30 DK090744","P30DK090744","K99 DK101585","5P01DK057751","P30 DK034989"],"pubmed_authors":["Duong SL","Kuo IY","Ehrlich BE","Nguyen L"],"additional_accession":[]},"is_claimable":false,"name":"Decreased Polycystin 2 Levels Result in Non-Renal Cardiac Dysfunction with Aging.","description":"Mutations in the gene for polycystin 2 (Pkd2) lead to polycystic kidney disease, however the main cause of mortality in humans is cardiac related. We previously showed that 5 month old Pkd2+/- mice have altered calcium-contractile activity in cardiomyocytes, but have preserved cardiac function. Here, we examined 1 and 9 month old Pkd2+/- mice to determine if decreased amounts of functional polycystin 2 leads to impaired cardiac function with aging. We observed changes in calcium handling proteins in 1 month old Pkd2+/- mice, and these changes were exacerbated in 9 month old Pkd2+/- mice. Anatomically, the 9 month old Pkd2+/- mice had thinner left ventricular walls, consistent with dilated cardiomyopathy, and the left ventricular ejection fraction was decreased. Intriguingly, in response to acute isoproterenol stimulation to examine ?-adrenergic responses, the 9 month old Pkd2+/- mice exhibited a stronger contractile response, which also coincided with preserved localization of the ?2 adrenergic receptor. Importantly, the Pkd2+/- mice did not have any renal impairment. We conclude that the cardiac-related impact of decreased polycystin 2 progresses over time towards cardiac dysfunction and altered adrenergic signaling. These results provide further evidence that polycystin 2 provides a critical function in the heart, independent of renal involvement.","dates":{"release":"2016-01-01T00:00:00Z","publication":"2016","modification":"2021-02-21T02:06:55Z","creation":"2019-03-26T22:53:49Z"},"accession":"S-EPMC4833351","cross_references":{"pubmed":["27081851"],"doi":["10.1371/journal.pone.0153632"]}}