Ectopic expression of Cux1 is associated with reduced p27 expression and increased apoptosis during late stage cyst progression upon inactivation of Pkd1 in collecting ducts
| Autor: | Gregory G. Germino, Lynn Magenheimer, Carol G. Carlton, Gregory B. Vanden Heuvel, Dianne Vassmer, Binu M. Paul, Klaus Piontek, Aaron Taylor |
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| Rok vydání: | 2011 |
| Předmět: |
Male
TRPP Cation Channels Down-Regulation Kidney development Apoptosis Mice Transgenic Biology Transfection Article Andrology Mice Polycystic kidney disease medicine Animals Cyst Gene Silencing Kidney Tubules Collecting Homeodomain Proteins PKD1 Cell growth Nuclear Proteins Kidney Diseases Cystic medicine.disease Embryonic stem cell Up-Regulation Cell biology Enzyme Activation Repressor Proteins Animals Newborn Gene Expression Regulation Disease Progression Female Ectopic expression Cyclin-Dependent Kinase Inhibitor p27 Developmental Biology |
| Zdroj: | Developmental Dynamics. 240:1493-1501 |
| ISSN: | 1058-8388 |
| DOI: | 10.1002/dvdy.22625 |
| Popis: | Polycystic kidney diseases (PKD) are inherited disorders characterized by fluid-filled cysts primarily in the kidneys. We previously reported differences between the expression of Cux1, p21, and p27 in the cpk and Pkd1 null mouse models of PKD. Embryonic lethality of Pkd1 null mice limits its study to early stages of kidney development. Therefore, we examined mice with a collecting duct specific deletion in the Pkd1 gene. Cux1 was ectopically expressed in the cyst lining epithelial cells of newborn, P7 and P15 Pkd1CD mice. Cux1 expression correlated with cell proliferation in early stages of cystogenesis, however, as the disease progressed, fewer cyst lining cells showed increased cell proliferation. Rather, Cux1 expression in late stage cystogenesis was associated with increased apoptosis. Taken together, our results suggest that increased Cux1 expression associated with apoptosis is a common feature of late stage cyst progression in both the cpk and Pkd1CD mouse models of PKD. Developmental Dynamics 240:1493–1501, 2011. © 2011 Wiley-Liss, Inc. |
| Databáze: | OpenAIRE |
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