| First Author | Hu C | Year | 2022 |
| Journal | Physiol Rep | Volume | 10 |
| Issue | 5 | Pages | e15206 |
| PubMed ID | 35274831 | Mgi Jnum | J:328673 |
| Mgi Id | MGI:7257454 | Doi | 10.14814/phy2.15206 |
| Citation | Hu C, et al. (2022) Profiling renal sodium transporters in mice with nephron Ift88 disruption: Association with sex, cysts, and blood pressure. Physiol Rep 10(5):e15206 |
| abstractText | Loss of nephron primary cilia due to disruption of the Ift88 gene results in sex- and age-specific phenotypes involving renal cystogenesis, blood pressure (BP) and urinary Na(+) excretion. Previous studies demonstrated that male mice undergoing induction of nephron-specific Ift88 gene disruption at 2 months of age developed reduced BP and increased salt-induced natriuresis when pre-cystic (2 months post-induction) and became hypertensive associated with frankly cystic kidneys by 9 months post-induction; in contrast, female Ift88 KO mice manifested no unique phenotype 2 months post-induction and had mildly reduced BP 9 months post-induction. The current study utilized these Ift88 KO mice to investigate associated changes in renal Na(+) transporter and channel protein expression. At 2 months post-induction, pre-cystic male Ift88 KO mice had reduced high salt diet associated total NKCC2 levels while female mice had no alterations in Na(+) transporters or channels. At 9 months post-induction, cystic male Ift88 KO mice had increased total and phosphorylated NHE3 levels together with reduced NKCC2, phosphorylated and/or total NCC, and ENaC-alpha expression on normal and high salt diets. In contrast, female Ift88 KO mice at 9 months post-induction had no changes in Na(+) transporters or channels beyond an increase in phosphorylated-NCC during high salt intake. Thus, reduced BP in pre-cystic, and elevated BP in renal cystic, male Ift88 KO mice are associated with unique sex-dependent changes in nephron Na(+) transporter/channel expression. |
