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Expression analysis of effect of Intestine-specific knockdown of KLF5 on radiation induced intestinal injury

ABSTRACT: The objective was to determine the role of Krüppel-like factor 5 (KLF5) in radiation-induced intestinal injury. Mice with intestinal-specific knockdown of KLF5 (Cre+ mice) were generated and their response to radiation was compared with controls (Cre- mice). Mice were given 15 Gy total body irradiation (TBI). The mice intestines were harvested at 6h post TBI and screened for differentially expressed genes by microarray analysis. We identified 11,004 and 2,466 differentially expressed genes in non-irradiated and irradiated mice at 6h post TBI, respectively. KLF5 knockdown down-regulated genes related to DNA damage repair pathways such as nucleotide excision repair, mismatch repair, non-homologous end joining and the Fanconi anemia pathway, which may suggest a novel function of KLF5.

ORGANISM(S): Mus musculus

PROVIDER: GSE66655 | GEO | 2015/03/10

SECONDARY ACCESSION(S): PRJNA277629

REPOSITORIES: GEO

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Expression analysis of effect of Intestine-specific knockdown of KLF5 on radiation induced intestinal injury

Project description:The objective was to determine the role of Krüppel-like factor 5 (KLF5) in radiation-induced intestinal injury. Mice with intestinal-specific knockdown of KLF5 (Cre+ mice) were generated and their response to radiation was compared with controls (Cre- mice). Mice were given 15 Gy total body irradiation (TBI). The mice intestines were harvested at 6h post TBI and screened for differentially expressed genes by microarray analysis. We identified 11,004 and 2,466 differentially expressed genes in non-irradiated and irradiated mice at 6h post TBI, respectively. KLF5 knockdown down-regulated genes related to DNA damage repair pathways such as nucleotide excision repair, mismatch repair, non-homologous end joining and the Fanconi anemia pathway, which may suggest a novel function of KLF5. A four chip study using total RNA recovered from four pooled intestine tissues of four experimental groups. The four experimental groups respectively were the 6h-cre+ group, 6h-cre- group, con-cre+ group and con-cre- group. Equal mass amounts of total RNA were pooled from each small intestine to yield a sample representing RNA from 3 separate mice in each group. One pooled sample in every group were tested with one chip. Each chip measures the expression level of 44,170 genes from C57BL/6 mouse (background) with three 60-mer probe pairs per gene.

2015-03-10 | E-GEOD-66655 | biostudies-arrayexpress

Effect of cardiomyocyte KLF5 deletion in cardiac gene expression profile

Project description:Kruppel-like factor 5 gene was deleted (Cre-lox) system specifically in cardiomyocytes (aMHC-promoter-driven expression of Cre) and RNA was purified from total hearts (TRIZOL method) following perfusion of the heart with PBS. Basal levels cardiac RNA was analyzed with whole genome microarray chips. There were two groups of mice: 4 mice that had KLF5 gene floxed without expressing Cre recombinase (control group) and 4 mice that were expressing Cre in cardiomyocytes and therefore KLF5 gene was deleted and thus not expressed in this particular cell type.

2014-12-05 | E-GEOD-63839 | biostudies-arrayexpress

RNA-seq on biliary epithelial cells (BECs) of Klf5 LKO mice upon DDC injury

Project description:In other to assess functional involvement of Klf5 in DR regulation, we made liver-specific Klf5 knockout mice. Ductular reaction upon cholestatic liver injury is severely suppressed in these mice. We conducted RNA-seq analysis on the BECs from control mice and Klf5 LKO mice upon DDC injury to further elucidate the Klf5 functions.

2018-03-16 | GSE97167 | GEO

6 Gy gamma-irradiation of mouse small intestinal organoids at 24h, 48h and 96h after irradiation

Project description:The intact intestinal epithelial barrier protects our body from a range of immune mediated diseases. The epithelial layer has an impressive ability to reconstitute and repair upon damage and this process of repair is increasingly seen as a therapeutic target. In vitro models to study this process in primary intestinal cells are lacking. Therefore we established and characterized an in vitro model of intestinal damage and repair by applying γ-radiation on small intestinal organoids. We then used this model to identify novel regulators of intestinal regeneration. Small intestinal single crypts were isolated from C57BL/6 mice and cultured in matrigel. We treated the organoid cultures, 3 days after seeding, with 6 Gy of gamma-irradiation. RNA was isolated at 24, 48 and 96 hours after irradiation. Non-irradiated controls were collected per time point.

2019-12-06 | GSE141515 | GEO

Discovering radiation biomarkers in plasma of total-body irradiated leukemia patients

Project description:The population's increasing risk of acute large-scale radiological/nuclear exposures underlines the need for functional radiation biomarkers. As ionizing radiation triggers a complex response on the genome, proteome, and metabolome level, all were already reported as suitable indicators of radiation-induced damage in vitro or in animal models. We aim to analyze the blood of total-body irradiated (TBI) leukaemia patients using a mass spectrometry approach and to identify and quantify plasma proteins before and after irradiation. Combining two independent mass spectrometry approaches we identified 15 plasma proteins differing in the blood of TBI patients before and after irradiation. The majority of proteins were associated with the inflammatory responce of the immune system and with metabolism of lipids. These candidate radiation biomarkers might have implications for practical biological dosimetry.

2024-06-16 | PXD043516 | Pride

Differential gene expression in intestinal mouse crypts after loss of KLF5

Project description:To determine potential targets of KLF5 we performed RNA-sequencing on jejunal crypts isolated from Klf5-deficient and wildtype mice, using three biological replicates per genotype. We identified 1,480 genes that showed significant differential expression with at least a 2-fold difference between Klf5-deficient and wildtype (q-value â¤ 0.05) (Figure 5A; Supplementary Table 1). Klf5 expression was significantly downregulated 2.7-fold. Comparison of gene expression after loss of KLF5 in the intestine. Isolated jejunal crypts from 3 wildtype and 3 knockout animals were compared.

2016-04-01 | E-GEOD-79758 | biostudies-arrayexpress

Differential gene expression in intestinal mouse crypts after loss of KLF5

Project description:To determine potential targets of KLF5 we performed RNA-sequencing on jejunal crypts isolated from Klf5-deficient and wildtype mice, using three biological replicates per genotype. We identified 1,480 genes that showed significant differential expression with at least a 2-fold difference between Klf5-deficient and wildtype (q-value ≤ 0.05) (Figure 5A; Supplementary Table 1). Klf5 expression was significantly downregulated 2.7-fold.

2016-04-01 | GSE79758 | GEO

Genomic DNA copy number aberration in chromosome 18 of small intestinal tumors in B6/B6-Chr18MSM-F1 ApcMin/+ mice irradiated with ionizing radiation

Project description:To investigate DNA copy number changes in chromosome 18 of small intestinal tumors in B6/B6-Chr18MSM-F1 ApcMin/+ mice irradiated with ionizing radiation

2023-10-02 | GSE206669 | GEO

Expression data from conditional Klf5 knockout Pten-null mouse prostates

Project description:KLF5 is a basic transcription factor that regulates multiple biological processes, but its function in tumorigenesis appears contradictory in the current literature, with some studies showing tumor suppressor activity and others showing tumor promoting activity. In this study, we examined the function of Klf5 in prostatic tumorigenesis using mice with prostate specific deletion of Klf5 and Pten, both of which are frequently deleted in human prostate cancer. Histological and molecular analyses demonstrated that when one Pten allele was deleted, which causes mouse intraepithelial neoplasia (mPIN), Klf5 deletion accelerated the emergence and progression of mPIN. When both Pten alleles were deleted, which causes prostate cancer, Klf5 deletion promoted tumor growth and caused more severe morphological and molecular alterations, and homozygous deletion of Klf5 was more effective than hemizygous deletion. Unexpectedly, while Klf5 deletion clearly promoted tumorigenesis in luminal cells, it actually diminished the numbers of Ck5-positive basal cells in the Pten-null tumors. Klf5 deletion also increased the cell proliferation rate in tumors with Pten deletion, which involved extensive activation of the PI3K/AKT and MAPK mitogenic signaling pathways and inactivation of the p15 cell cycle inhibitor. Global gene expression and pathway analyses demonstrated that multiple mechanisms could be responsible for the tumor promoting effect of Klf5 deletion, We used microarrays to detail the global programme of gene expression of Klf5-wildtype and Klf5-null mouse dorsal prostates under Pten-null context to figure out the differential expression profiling underlying tumorigenesis 4 Klf5-wildtype and 4 Klf5-null mouse (6 months age) dorsal prostates under Pten-null context were used for RNA extraction and hybridization on Affymetrix mouse st 1.0 array

2014-06-21 | E-GEOD-58719 | biostudies-arrayexpress

Over-expression and knockdown of KLF5

Project description:Activation of the Ras/Erk pathway upregulates expression of the Kruppel-like Factor 5 (KLF5) transcription factor, and KLF5 is a downstream mediator of Ras oncogenic signaling. Specifically, in bladder and colon cancer cell lines KLF5 upregulates the Ras-pathway target gene cyclin D1, and facilitates entry into the S phase of the cell cycle. Ras mutations are common in lung cancer, but a role for KLF5 in lung tumorigenesis has not been defined. To this end, we manipulated KLF5 expression in four Ras-mutant human lung adenocarcinoma cell lines to find that KLF5 significantly modulates anchorage-independent growth, a mutant Ras phenotype. However, in a mouse model of human lung adenocarcinoma, K-RasG12D does not critically require Klf5 to mediate oncogenesis or induce cyclin D1 expression. Patients with lung tumors expressing high levels of KLF5 have significantly better prognosis than those with low or no KLF5 expression (opposite of mutant Ras prognosis). The latter may be explained by KLF5 transcriptional repression of the ATP-binding cassette, sub-family G (WHITE), member 2 (ABCG2), an anthracycline transporter. In agreement with this, KLF5 knockdown cells display significantly more Hoechst “side population” and resistance to doxorubicin. In summary, while KLF5 is not an obligate partner in Ras oncogenic signaling, KLF5 control of ABCG2 expression is significant to patient survival.

2010-06-23 | GSE16555 | GEO

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