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Expression data from mouse livers expressing or lacking Cre recombinase during pneumonia

ABSTRACT: Cre-recombinase expression under control of an albumin promoter in the presence of floxed alleles is a highly effective and specific way to target gene mutations in hepatocytes. However, some concerns have been raised regarding off-target and/or toxic effects of cre itself, possibly confounding the interpretation of studies employing this approach. We have now used this tool to succesfully target gene deletions in hepatocytes during pneumonia, a condition which results in significant remodeling of the hepatic transcriptome. The goal of this study was to determine what effects, if any, cre expression alone has on hepatic gene expression during bacterial pneumonia. Mutant mice expressed CRE-recombinase under control of an albumin promoter. Results from mutants were compared to wild-type mice on the same genetic background (C57BL/6). Microarray analysis was performed on liver RNA collected from both genotypes of mice in the absence and presence of pneumococcal pneumonia.

ORGANISM(S): Mus musculus

PROVIDER: GSE35515 | GEO | 2012/02/16

SECONDARY ACCESSION(S): PRJNA156111

REPOSITORIES: GEO

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Expression data from mouse livers expressing or lacking Cre recombinase during pneumonia

Project description:Cre-recombinase expression under control of an albumin promoter in the presence of floxed alleles is a highly effective and specific way to target gene mutations in hepatocytes. However, some concerns have been raised regarding off-target and/or toxic effects of cre itself, possibly confounding the interpretation of studies employing this approach. We have now used this tool to succesfully target gene deletions in hepatocytes during pneumonia, a condition which results in significant remodeling of the hepatic transcriptome. The goal of this study was to determine what effects, if any, cre expression alone has on hepatic gene expression during bacterial pneumonia. Mutant mice expressed CRE-recombinase under control of an albumin promoter. Results from mutants were compared to wild-type mice on the same genetic background (C57BL/6). Microarray analysis was performed on liver RNA collected from both genotypes of mice in the absence and presence of pneumococcal pneumonia. RNA from 2 separate groups of mice (3 mice per group) was analyzed: 1) Control mice infected intratracheally for 24h with 10^6 CFU of Streptococcus pneumoniae (serotype 3); and 2) Mutant mice infected intratracheally for 24h with 10^6 CFU of Streptococcus pneumoniae (serotype 3).

2012-02-16 | E-GEOD-35515 | biostudies-arrayexpress

Expression data from mouse livers lacking STAT3 during pneumonia

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Expression data from mouse livers lacking NF-kappaB RelA (p65) during pneumonia

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Expression data from mouse livers lacking STAT3 and RelA during pneumonia

Project description:A common response to physiological duress is the hepatic acute phase response, a process during which the expression of many genes is altered in the liver. Amongst these transcripts are those encoding acute phase proteins, defined as circulating proteins with significantly changed concentrations during an acute phase response. The goal of this study was to determine the influence of two transcription factors, STAT3 and NF-kappaB p65 (RelA), on hepatic gene changes including but not limited to acute phase proteins during bacterial pneumonia. Using the Cre-LoxP system, mice were generated with combined functional deletions of both STAT3 and RelA in hepatocytes. In mutant mice, Cre-recombinase was expressed under transcriptional control of an albumin promoter in the presence of homozygous floxed alleles for both STAT3 and RelA. Wild-type control mice lacked the Cre-recombinase transgene. Microarray analysis was performed on liver RNA collected from both genotypes of mice in the absence and presence of pneumococcal pneumonia.

2012-02-16 | GSE32105 | GEO

Expression data from mouse livers lacking STAT3 during pneumonia

Project description:A common response to physiological duress is the hepatic acute phase response, a process during which the expression of many genes is altered in the liver. Amongst these transcripts are those encoding acute phase proteins, defined as circulating proteins with significantly changed concentrations during an acute phase response. The goal of this study was to determine the influence of STAT3 on hepatic gene changes including but not limited to acute phase proteins during bacterial pneumonia. Using the Cre-LoxP system, mice were generated with functional deletion of STAT3 in hepatocytes. In mutant mice, Cre-recombinase was expressed under transcriptional control of an albumin promoter in the presence of homozygous floxed alleles for STAT3. Wild-type control mice lacked the Cre-recombinase transgene. Microarray analysis was performed on liver RNA collected from both genotypes of mice in the absence and presence of pneumococcal pneumonia. RNA from 2 separate groups of mice (3 mice per group) was analyzed: 1) Control mice infected intratracheally for 24h with 10^6 CFU of Streptococcus pneumoniae (serotype 3); and 2) Mutant mice infected intratracheally for 24h with 10^6 CFU of Streptococcus pneumoniae (serotype 3).

2012-02-16 | E-GEOD-35514 | biostudies-arrayexpress

Expression data from mouse livers lacking NF-kappaB RelA (p65) during pneumonia

Project description:A common response to physiological duress is the hepatic acute phase response, a process during which the expression of many genes is altered in the liver. Amongst these transcripts are those encoding acute phase proteins, defined as circulating proteins with significantly changed concentrations during an acute phase response. The goal of this study was to determine the influence of NF-kappaB RelA (p65) on hepatic gene changes including but not limited to acute phase proteins during bacterial pneumonia. Using the Cre-LoxP system, mice were generated with functional deletion of NF-kappaB RelA (p65) in hepatocytes. In mutant mice, Cre-recombinase was expressed under transcriptional control of an albumin promoter in the presence of homozygous floxed alleles for RelA. Wild-type control mice lacked the Cre-recombinase transgene. Microarray analysis was performed on liver RNA collected from both genotypes of mice in the absence and presence of pneumococcal pneumonia. RNA from 2 separate groups of mice (3 mice per group) was analyzed: 1) Control mice infected intratracheally for 24h with 10^6 CFU of Streptococcus pneumoniae (serotype 3); and 2) Mutant mice infected intratracheally for 24h with 10^6 CFU of Streptococcus pneumoniae (serotype 3).

2012-02-16 | E-GEOD-35513 | biostudies-arrayexpress

Expression data from mouse livers lacking STAT3 and RelA during pneumonia

2012-02-16 | E-GEOD-32105 | biostudies-arrayexpress

Mouse livers lacking NF-kappaB RelA (p65) during bacteremia

Project description:Using a mouse model with hepatocyte-specific deletion of transcription factor NF-κB RelA (p65), our group has previously revealed the important role of RelA in inducing the acute phase response, maintaining host defense, and preventing liver injury during sepsis. To goal of this study was determine the influence of RelA on hepatic gene changes that provide liver protection during infection. Mice were generated with functional deletion of NF-kappaB RelA (p56) in hepatocytes using a Cre-LoxP system. Mutant mice expressed Cre-recombinase under the transcriptional control of an albumin promotor and homozygous floxed RelA alleles. Wild type control mice lack the Cre-recombinase. Microarray analysis was performed on liver RNA collected from both genotypes of mice in the absence and presence of pneumococcal bacteremia.

2019-06-07 | GSE126642 | GEO

Comparison of Ildr2 knockdown by (Adv-shRNA) and Ildr2 knockout (Adv-Cre) in mouse liver

Project description:We observed that Ildr2 knockdown via adenovirally-delivered shRNA (Adv-Ildr2 shRNA) causes hepatic steatosis in mice. Acute, liver-specific Ildr2 knockout mice generated by infecting C57BL/6J mice segregating for a floxed allele of Ildr2 with adenoviral Cre recombinase (Adv-Cre) do not develop hepatic steatosis. However, administration of Adv-Ildr2 shRNA to Ildr2 knockout mice (Ildr2floxed; albumin-cre) did cause hepatic steatosis, indicating that the Adv-Ildr2 shRNA had apparent “off-target” effects on gene(s) other than Ildr2. To determine additional targets of Ildr2 shRNA that may regulate hepatic lipid metabolism, we performed RNA sequencing on liver samples from (1) Adv-Ildr2 shRNA knockdown mice, (2) Adv-lacZ shRNA control mice, and (3) Adv-Cre Ildr2 knockout mice. For the purposes of our study, we sought to identify genes downregulated by Adv-Ildr2 shRNA, but unchanged in Adv-lacZ shRNA control or Adv-Cre Ildr2 knockout mice. The hepatic steatosis observed in Adv-Ildr2 shRNA knockdown mice was likely due to shRNA targeting of other “off-target” genes. We propose that the genes candidates identified in this sequencing experiment may lead to identification of novel regulators of hepatic lipid metabolism.

2018-05-11 | GSE114289 | GEO

Cre-recombinase expression cooperates with FLT3ITD/ITD to induce acute myeloid leukemia [RNASeq_SclCre_Spleen]

Project description:Animal models offer a valuable tool to recapitulate genetically defined subtypes of AML, and to assess the potential of compound mutations and clonal evolution during disease progression. This is of utmost importance for difficult to treat leukemias such as FLT3-ITD positive AML. While conditional gene targeting by Cre-recombinase is a powerful technology that has revolutionized biomedical research, consequences of Cre-expression such as lack of fidelity, toxicity or off-target effects need to be taken into consideration. We report on a transgenic murine model of FLT3-ITD induced disease, where Cre-recombinase expression alone, and in the absence of a conditional allele, gives rise to an aggressive leukemia phenotype. Here, expression of various Cre-recombinases leads to polyclonal expansion of FLT3ITD/ITD progenitor cells, induction of a differentiation block and activation of Myc-dependent gene expression programs. Our report is intended to alert the scientific community of potential risks associated with using this specific mouse model and of unexpected effects of Cre-expression when investigating cooperative oncogenic mutations in murine models of cancer.

2023-02-08 | GSE212221 | GEO

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