Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

Expression data from tamoxifen treated and control injection treated Tg(αMHC-MerCreMer) and wild type mus musculus.

ABSTRACT: α-myosin heavy chain promoter controlled MerCreMer expression enables conditional, cardiomyocyte specific and tamoxifen dependent gene inactivation of floxed genes. Administration of tamoxifen has been linked to development of acute and transient cardiomyopathy. The mechanism for this is unknown. We used microarrays to sort out factors relevant for adverse effects following tamoxifen dependent gene inactivation, to develop a protocol with minimal adverse effects, and to identify the most proper control animals. Mus musculus Tg(αMHC-MerCreMer) and wild type were sacrificed 4 days after 1 or 4 consecutive days of 40 mg/kg tamoxifen injected intraperitoneally, or after corresponding control injection treatment.

ORGANISM(S): Mus musculus

SUBMITTER: Karina Hougen

PROVIDER: E-GEOD-19344 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Project description:Although early developmental processes involve cell fate decisions that define the body axes and establish progenitor cell pools, development does not cease once cells are specified. Instead, most cells undergo specific maturation events where changes in the cell transcriptome ensure that the proper gene products are expressed to carry out unique physiological functions. Pancreatic acinar cells mature post-natally to handle an extensive protein synthetic load, establsih organized apical-basal polarity for zymogen granule trafficking, and assemble gap-junctions to perimt efficient cell-cell communication. Despite significant progress in defining transcriptional networks that control initial acinar cell specification and differentiation decisions, little is know regarding the role of transcription factors in the specification and maintenance of maturation events. One candidate maturation effector is MIST1, a secretory cell-restricted transcription factor that has been implicated in controlling regulated exocytosis events in a number of cell types. Embryonic knock-out of MIST1 generates acinar cells that fail to establish an apical-basal organization, fail to properly localize zymogen granule and fail to communicate intra-cellularly, making the exocrine organ highly suceptible to pancreatic diseases. In an effort to identify the gene expression differences responsible for MIST1 regulating mature acinar properties. We generated a tamoxifen-inducible mouse model where MIST1 expression could be activated in vivoand performed gene expression arrays on wildtype, MIST1-null, and induced MIST1 pancreatic RNA. RNA was isolated from pancreata of 8 week old mice using the Qiagen RNeasy Midi kit. Pancreta of wildtype, MIST1-null, and MIST1-null with a tamoxifen inducible MIST1-expressing transgene were harvested 36 hours post-tamoxifen administration. Therefore, this experiment provides information on steady-state gene expression differences between wildtype and MIST1-null mice as well as immediate gene expression changes induced by MIST1 expression.

Dataset Information

Expression data from tamoxifen treated and control injection treated Tg(αMHC-MerCreMer) and wild type mus musculus.

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