Gene expression profiling in the remnant kidney model of wild type and kinin B1 and B2 receptor knockout mice

Schanstra, Joost P.; Bachvarova, Magdalena; Neau, Eric; Bascands, Jean-Loup; Bachvarov, Dimcho

doi:10.1038/sj.ki.5002172

Cited by 20 publications

(15 citation statements)

References 56 publications

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“…Microarray analysis was performed according to established protocols (Schanstra et al, 2007). Briefly, fluorescently labeled cRNA was generated from 0.5 μg total RNA in each reaction using the Agilent Fluorescent Direct Label Kit and 1.0 mM Cyanine 3′-or 5′-labeled dCTP (PerkinElmer).…”

Section: Genome-wide Microarray Analysismentioning

confidence: 99%

“…Hybridization was performed using the Oligonucleotide Microarray Hybridization and In Situ Hybridization Plus Kit (Agilent). The labeled cRNA was hybridized to Agilent 44K whole mouse genome oligonucleotide microarray (containing ∼41,000 probes) as previously described (Schanstra et al, 2007). The arrays were scanned using a duallaser DNA microarray scanner (Agilent).…”

Section: Genome-wide Microarray Analysismentioning

confidence: 99%

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Histone deacetylase 1 and 2 regulate Wnt and p53 pathways in the ureteric bud epithelium

Chen

Xiao

et al. 2015

Development

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Histone deacetylases (HDACs) regulate a broad range of biological processes through removal of acetyl groups from histones as well as non-histone proteins. Our previous studies showed that Hdac1 and Hdac2 are bound to promoters of key renal developmental regulators and that HDAC activity is required for embryonic kidney gene expression. However, the existence of many HDAC isoforms in embryonic kidneys raises questions concerning the possible specificity or redundancy of their functions. We report here that targeted deletion of both the Hdac1 and Hdac2 genes from the ureteric bud (UB) cell lineage of mice causes bilateral renal hypodysplasia. One copy of either Hdac1 or Hdac2 is sufficient to sustain normal renal development. In addition to defective cell proliferation and survival, genome-wide transcriptional profiling revealed that the canonical Wnt signaling pathway is specifically impaired in UB Hdac1,2−/− kidneys. Our results also demonstrate that loss of Hdac1 and Hdac2 in the UB epithelium leads to marked hyperacetylation of the tumor suppressor protein p53 on lysine 370, 379 and 383; these post-translational modifications are known to boost p53 stability and transcriptional activity. Genetic deletion of p53 partially rescues the development of UB Hdac1,2−/− kidneys. Together, these data indicate that Hdac1 and Hdac2 are crucial for kidney development. They perform redundant, yet essential, cell lineage-autonomous functions via p53-dependent and -independent pathways.

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Section: Genome-wide Microarray Analysismentioning

confidence: 99%

Section: Genome-wide Microarray Analysismentioning

confidence: 99%

Histone deacetylase 1 and 2 regulate Wnt and p53 pathways in the ureteric bud epithelium

Chen

Xiao

et al. 2015

Development

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“…Genome-wide Microarray Analysis-Microarray analysis was performed according to established protocols (50). The results represent three separate microarray experiments.…”

Section: Rt-pcr and Real Time Rt-pcr-totalmentioning

confidence: 99%

“…Hybridization was performed using the oligonucleotide microarray hybridization and in situ hybridization plus kit from Agilent (following the owner's manual). The labeled cRNA was hybridized to Agilent 44K whole mouse genome oligonucleotide microarray (containing ϳ41,000 Probes) as described previously (50). The arrays were scanned using a dual-laser DNA microarray scanner (Agilent).…”

Section: Rt-pcr and Real Time Rt-pcr-totalmentioning

confidence: 99%

Histone Deacetylase (HDAC) Activity Is Critical for Embryonic Kidney Gene Expression, Growth, and Differentiation

Chen

Bellew

Xiao

et al. 2011

Journal of Biological Chemistry

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Histone deacetylases (HDACs) regulate fundamental biological processes such as cellular proliferation, differentiation, and survival via genomic and nongenomic effects. This study examined the importance of HDAC activity in the regulation of gene expression and differentiation of the developing mouse kidney. Class I HDAC1-3 and class II HDAC4, -7, and -9 genes are developmentally regulated. Moreover, HDAC1-3 are highly expressed in nephron precursors. Short term treatment of cultured mouse embryonic kidneys with HDAC inhibitors (HDACi) induced global histone H3 and H4 hyperacetylation and H3K4 hypermethylation. However, genome-wide profiling revealed that the HDAC-regulated transcriptome is restricted and encompasses regulators of the cell cycle, Wnt/␤-catenin, TGF-␤/Smad, and PI3K-AKT pathways. Further analysis demonstrated that base-line expression of key developmental renal regulators, including Osr1, Eya1, Pax2/8, WT1, Gdnf, Wnt9b, Sfrp1/2, and Emx2, is dependent on intact HDAC activity. Treatment of cultured embryonic kidney cells with HDACi recapitulated these gene expression changes, and chromatin immunoprecipitation assays revealed that HDACi is associated with histone hyperacetylation of Pax2/Pax8, Gdnf, Sfrp1, and p21. Gene knockdown studies demonstrated that HDAC1 and HDAC2 play a redundant role in regulation of Pax2/8 and Sfrp1 but not Gdnf. Long term treatment of embryonic kidneys with HDACi impairs the ureteric bud branching morphogenesis program and provokes growth arrest and apoptosis. We conclude that HDAC activity is critical for normal embryonic kidney homeostasis, and we implicate class I HDACs in the regulation of early nephron gene expression, differentiation, and survival.Kidney development depends on reciprocal inductive interactions between the metanephric mesenchyme (MM), 4 a specified region in the caudal intermediate mesoderm, and the ureteric bud (UB), an epithelial outgrowth from the Wolffian (nephric) duct (1-3). Recent years have witnessed significant progress in our understanding of the gene regulatory networks of early kidney development (3-6). For example, the Osr1/ Eya1/Pax2/Six/Sall/WT1/Hoxd11 gene regulatory network specifies the MM and is absolutely required for expression of glia-derived neurotrophic factor (Gdnf) (7,8). Gdnf, in turn, is essential for UB outgrowth and subsequent branching (9 -11).Gdnf acts via activation of a c-Ret/PI3K/ERK-dependent gene network (Wnt11, Spry1, Etv4, Etv5, Cxcr4, Myb, Met, and Mmp14) in UB tip cells to control the branching morphogenesis program (12-14). Various growth factor/receptor signaling pathways, including FGFs, bone morphogenic proteins, VEGF, semaphorins, hepatocyte growth factor, EGF, among others, share signaling components with the c-Ret pathway and are required for optimal metanephric growth and patterning (15)(16)(17)(18)(19)(20)(21)(22). Following induction of the MM, activation of the Wnt/␤-catenin signaling pathway plays a key role in nephrogenesis. Release of Wnt9b from the UB branches triggers a ␤-catenindependent mo...

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“…Several studies suggest that Fabp1 is not expressed in both mouse and rat kidney in normal and pathophysiological conditions [30]. However, a recent study indicates that Fabp1 is expressed in the kidney [31]. Importantly, several clinical studies demonstrated the significance of urinary Fabp1 in kidney diseases.…”

Section: Discussionmentioning

confidence: 99%

Identification of Genes Related to the Early Stage of Angiotensin II-induced Acute Renal Injury by Microarray and Integrated Gene Network Analysis

Zhang¹,

Zhang²,

Wang³

et al. 2014

Cell Physiol Biochem

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Background/Aims: Angiotensin II (Ang II) mediated signaling plays a key role in the development of chronic kidney damage that contributes to renal fibrosis. However, the gene expression changes regulated by Ang II in the early stage of acute renal injury remain unclear. Methods: C57BL/6 wild-type (WT) mice were injected with Ang II (1500 ng/kg/min) for 1, 3 and 7 days. A time series analysis of microarrays was performed to evaluate Ang II-induced differentially gene expression in the kidneys. The data of gene expression in the kidney was further dissected by ANOVA analysis, gene expression profiles, gene network construction and quantitative real-time RT-PCR. Ang II-induced renal inflammation and fibrosis in mice were confirmed by pathological examination. Results: Our microarray data showed that a total of 1,511 differentially expressed genes were identified in the kidneys at 1, 3 and 7 days after Ang II infusion. These genes function in multiple biological processes, including response to stimuli, immune response, cell adhesion, metabolic process, kidney development, regulation of blood pressure, and ion transport, which may play critical roles in the pathobiology of Ang II-induced acute renal injury at the early stage. Furthermore, among these genes, 20 genes were further selected for final investigation. The dynamic gene network analysis demonstrated that fatty acid binding protein 1 (Fabp1) localized in the core of the network. Conclusions: Our data suggests that genes involved in lipid metabolic process, especially Fabp1, may play a central role in the development of Ang II-induced acute renal injury at the early stage.

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Gene expression profiling in the remnant kidney model of wild type and kinin B1 and B2 receptor knockout mice

Cited by 20 publications

References 56 publications

Histone deacetylase 1 and 2 regulate Wnt and p53 pathways in the ureteric bud epithelium

Histone deacetylase 1 and 2 regulate Wnt and p53 pathways in the ureteric bud epithelium

Histone Deacetylase (HDAC) Activity Is Critical for Embryonic Kidney Gene Expression, Growth, and Differentiation

Identification of Genes Related to the Early Stage of Angiotensin II-induced Acute Renal Injury by Microarray and Integrated Gene Network Analysis

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