Unknown,Transcriptomics,Genomics,Proteomics

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Mouse embryonic kidneys (E13.5): mutant (UB HDAC1,2-/-) vs. wild type

ABSTRACT: Transcriptional profiling of mouse embryonic kidneys (E13.5) comparing UB HDAC1,2-/- kidneys with wild type kidneys. Studies in our lab showed that histone deacetylase 1 (HDAC1) and 2 (HDAC2) perform redundant, yet essential functions in the developing mouse ureteric bud (UB) tissue. Double deletion of HDAC1 and HDAC2 in the UB results in impaired UB branching morphogenesis, followed by severe kidney dysgenesis. The goal of the microarray analysis was to identify the genetic pathways controlled by HDAC1 and 2 in the UB. Two-condition experiment: E13.5 mutant kidneys (UB HDAC1,2-/-) vs. E13.5 wild type kidneys . Biological replicates: 4 control replicates, 4 UB HDAC1,2-/- replicates. Two-color Agilent 4x44k chips with dye-swaps on 2 of 4 arrays.

ORGANISM(S): Mus musculus

SUBMITTER: Samir El-Dahr

PROVIDER: E-GEOD-35432 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Project description:Histone deacetylases (Hdac) remove acetyl groups from proteins, influencing global and specific gene expression. Hdacs control inflammation, as shown by Hdac inhibitor-dependent protection from DSS-induced murine colitis. While tissue-specific Hdac knockouts show redundant and specific functions, little is known of their intestinal epithelial cell (IEC) role. We have shown previously that dual Hdac1/Hdac2 IEC-specific loss disrupts cell proliferation and determination, with decreased secretory cell numbers and altered barrier function. We thus investigated how compound Hdac1/Hdac2 or Hdac2 IEC-specific deficiency alters the inflammatory response. Floxed Hdac1 and Hdac2 and villin-Cre mice were interbred. Compound Hdac1/Hdac2 IEC-deficient mice showed chronic basal inflammation, with increased basal Disease Activity Index (DAI) and deregulated Reg gene colonic expression. DSS-treated dual Hdac1/Hdac2 IEC-deficient mice displayed increased DAI, histological score, intestinal permeability and inflammatory gene expression. In contrast to double knockouts, Hdac2 IEC-specific loss did not affect IEC determination and growth, nor result in chronic inflammation. However, Hdac2 disruption protected against DSS colitis, as shown by decreased DAI, intestinal permeability and caspase-3 cleavage. Hdac2 IEC-specific deficient mice displayed increased expression of IEC gene subsets, such as colonic antimicrobial Reg3b and Reg3g mRNAs, and decreased expression of immune cell function-related genes. Our data show that Hdac1 and Hdac2 are essential IEC homeostasis regulators. IEC-specific Hdac1 and Hdac2 may act as epigenetic sensors and transmitters of environmental cues and regulate IEC-mediated mucosal homeostatic and inflammatory responses. Different levels of IEC Hdac activity may lead to positive or negative outcomes on intestinal homeostasis during inflammation Total RNAs from the colon of three control and three Hdac2 IEC-specific knockout mice were isolated with the Rneasy kit (Qiagen, Mississauga, ON, Canada).

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Mouse embryonic kidneys (E13.5): mutant (UB HDAC1,2-/-) vs. wild type

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