Project description:To elucidate the molecular mechanism of blood pressure regulation, we performed DNA microarray analyses to investigate gene expression in the kidneys of Cnnm2fl/fl;Six2-Cre mice.
Project description:To identify novel transcriptional targets following Qpc inactivation. We deleteted Qpc in SIX2 nephron progenitor cells using a Six2-eGFP/cre BAC transgene. We compared SIX2-expressing progenitors from Six2-Qpc-/- kidneys with control (Six2-Qpc+/-) embryonic kidneys at E18.5.
Project description:Glomerular RNA comparison between wild-type and podocyte specific deletion of the PTIP gene in 1 month old kidneys. The PTIP gene was deleted using a floxed allele and a Podocin-Cre driver strain. These mice develop protein urea by 3 months of age. This study was designed to find gene expression differences prior to the onset of the phenotype. A ptip floxed allele was crossed into the Podocin-Cre expressing strain to generate ptip fl/fl homozygous mice or ptip fl/- transheterozygous mice with or without the Cre expressing transgene. Animals were genotyped and assigend into two groups: Mutants with PTIP deletion (PTIP-) with the genotype ptip fl/fl:Pod-Cre or ptip fl/-:Pod-Cre or control mice (PTIP+) with either ptip fl/fl or ptip fl/-. Note that the floxed allele produced normal levels of wild-type PTIP protein. Kidneys were excised at 1 month of age. Glomeruli enriched fractions were generated by sieving of the tissue homogenates. RNA was prepared from glomerular enriched fractions.
Project description:In developing mammalian kidney, nephron progenitor cells (NPC) give rise to all cells in mature nephrons. Expression of the transcription factor Six2 marks NPC in developing mouse kidneys. Within the Six2+ cell population, uncommitted NPC is marked by Cited1 expression. Towards the depletion of NPC in P2, most of the Cited1+ NPC is committed. Therefore, most of the Six2+ cells in kidney represents committed NPC. In order to explore the mechanism of NPC self-renewal and differentiation, hereby we generated transcriptionl profiles of uncommitted NPC (Cited1RFP+ cells from kidneys of E16.5 Cited1tagRFP transgenic mice) and committed NPC (Six2GFP+ cells from kidneys of P2 Six2TGC transgenic mice).
Project description:To study the role of GC-A and p38MAPK in podocytes, we used microarray analysis and compared gene expression profiles of the glomerulus of GC-A fl/fl p38 fl/fl Nephrin-Cre(Cre/+) mice and GC-A fl/fl p38 fl/fl Nephrin-Cre (+/+) mice. GC-A: guanylyl cyclase-A
Project description:We created mice, which are deficient for Myc specifically in cardiac myocytes by crossing crossed Myc-floxed mice (Mycfl/fl) and MLC-2VCre/+ mice. Serial analysis of earlier stages of gestation revealed that Myc-deficient mice died prematurely at E13.5-14.5. Morphological analyses of E13.5 Myc-null embryos showed normal ventricular size and structure; however, decreased cardiac myocyte proliferation and increased apoptosis was observed. BrdU incorporation rates were also decreased significantly in Myc-null myocardium. Myc-null mice displayed a 3.67-fold increase in apoptotic cardiomyocytes by TUNEL assay. We examined global gene expression using oligonucleotide microarrays. Numerous genes involved in mitochondrial death pathways were dysregulated including Bnip3L and Birc2. Keywords: wildtype vs Myc-null
