ABSTRACT: Gene expression profiles of E15.5 cortical collecting duct and anlage of loop of Henle isolated from developing kidney using LCM. (GUDMAP Series ID: 18)
Project description:We profiled SUMO1 and SUMO2 modified proteins in cortical collecting duct (mpkCCD) as a precursor to targeted approaches to assess SUMO function. SUMO levels in cells following heat shock and treatment with deSUMOylation inhibitors were assessed.
Project description:To study the effects of aldosterone on miRNA in the kidney cortical collecting duct, polarized mpkCCDc14 cell were treated with aldosterone or vehicle. A putative target for miR-466g was identified, the effect of modulating miR-466g levels on SGK1 levels was examined
Project description:Purpose: Lithium salts, used for treatment of bipolar disorder, frequently induce nephrogenic diabetes insipidus (NDI), limiting therapeutic success. NDI is associated with loss of expression of the molecular water channel, aquaporin-2, in the renal collecting duct (CD). Here, we use the methods of systems biology in a well-established rat model of lithium-induced NDI to identify signaling pathways activated at the onset of polyuria. Methods: We carried out RNA-sequencing in cortical CDs microdissected from rats treated with lithium for 12-72 hours (vs. time controls). Administration of anti-inflammatory doses of dexamethasone to lithium-treated rats countered the loss of aquaporin-2 protein. Protein mass spectrometry in microdissected cortical CDs provided corroborative evidence, but also identified decreased abundance of several anti-oxidant proteins. Cortical thick ascending limbs of Henle were also microdissected for RNA-Seq at 72 hrs. We carried out RNA-Seq for 2-3 CCD sample per rat (1 lithium-treated rat versus 1 control at 12, 24, 36 hrs). Results and conclusion: Integration of new data with prior data about lithium effects at a molecular level leads to a signaling model in which lithium increases ERK activation leading to induction of NF-κB signaling and an inflammatory-like response that represses Aqp2 gene transcription.
Project description:Analysis of expression changes in renal collecting duct epithelial cells by adenoviral mediated Krüppel like transcription factor 5 (KLF5) overexpression. KLF5 is a key regulator of static and inflammatory stage in renal collecting duct epithelial cells. We thought these results provide insights into downstream genes of KLF5 in renal collecting duct epithelial cells.
