Browse
Submit Data
Databases
API
Help

Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

29 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Thrombopoietin (TPO) protects against heart damage induced by doxorubicin and infarction in rat models

ABSTRACT: In order to examine the mechanism of TPO on cardiac protection against DOX damage, we have employed whole genome microarray expression profiling as a discovery platform to identify genes with the potential to delineate the TPO cardioprotective mechanism against DOX-induced cardiomyopathy Dox and TPO induced gene expressions in rat heart were measured at day 6. Two biological replicates were performed for each treatment group.

ORGANISM(S): Rattus norvegicus

SUBMITTER: Kathy Chan

PROVIDER: E-GEOD-15449 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Publications

Thrombopoietin protects against doxorubicin-induced cardiomyopathy, improves cardiac function, and reversely alters specific signalling networks.

Chan Kathy Yuen-Yee KY Xiang Ping P Zhou Ligang L Li Karen K Ng Pak-Cheung PC Wang Chi-Chiu CC Zhang Lei L Deng Hai-Yan HY Pong Nga-Hin NH Zhao Hailu H Chan Wood-Yee WY Sung Rita Yn-Tz RY

European journal of heart failure 20110216 4

<h4>Aims</h4>We investigated the therapeutic efficacy of thrombopoietin (TPO) in acute and chronic rat models of heart damage and explored the mechanisms in terms of genome-wide transcriptional changes, phosphorylation signals, and bone marrow endothelial progenitor cell (EPC) levels.<h4>Methods and results</h4>Cardiac damage was induced in rat models of (i) acute-doxorubicin (DOX) treatment: single high-dose DOX, four doses TPO, followed up for 5 days; and (ii) chronic-DOX treatment: one low-do ...[more]

PMID: 21330293

Publication: 1/2

Similar Datasets

Thrombopoietin (TPO) protects against heart damage induced infarction in rat model

Project description:In order to examine the mechanism of TPO on cardiac protection against myocardial infarction damage (MI), we have employed whole genome microarray expression profiling as a discovery platform to identify genes with the potential to delineate the TPO cardioprotective mechanism against infarction. MI and TPO induced gene expressions in rat heart were measured at week 4. Two biological replicates were performed for each treatment group.

2012-12-01 | E-GEOD-22489 | biostudies-arrayexpress

Transcriptional profiling of murine bone marrow derived macrophages differentiated with macrophage colony-stimuating factor (M-CSF) or granulocyte-macrophage colony-stimulating factor (GM-CSF)

Project description:In this study, we compared murine bone marrow monocytes differentiated for 7 days with M-CSF or GM-CSF. A comparison of the different macrophage populations was made using microarray profiling. Threshold: 1.0 . Logbase: 2 . Technology: Agilent.SingleColor.14868. Normalization: Shift to 75 percentile . Baseline Transformation: median of all samples . FlagSettings:. Feature is not positive and significant:M. Feature is not above background:M. Feature is not Uniform:A. Feature is a population outlier:A. Feature is Saturated:A.

2012-03-20 | E-MTAB-790 | biostudies-arrayexpress

Transcriptional profiling of murine bone marrow-derived macrophages differentiated with macrophage colony-stimulating factor (M-CSF) and/or granulocyte-macrophage colony-stimulating factor (GM-CSF) for short term

Project description:In this study, we compared murine bone marrow monocytes differentiated for 7 days with M-CSF then BMM were cultured in the absence of M-CSF for 24hr (starved), then treated with different combinations of M-CSF, GM-CSF, TNF and Dex for 16hr. A comparison of the different macrophage populations was made using microarray profiling. Threshold: 1.0 . Logbase: 2 . Technology: Agilent.SingleColor.14868. Normalization: Shift to 75 percentile . Baseline Transformation: median of all samples . FlagSettings:. Feature is not Uniform:A. Feature is a population outlier:A. Feature is Saturated:A. Feature is not above background:M. Feature is not positive and significant:M.

2012-03-20 | E-MTAB-792 | biostudies-arrayexpress

Thrombopoietin (TPO) protects against heart damage induced by doxorubicin and infarction in rat models

Project description:In order to examine the mechanism of TPO on cardiac protection against DOX damage, we have employed whole genome microarray expression profiling as a discovery platform to identify genes with the potential to delineate the TPO cardioprotective mechanism against DOX-induced cardiomyopathy

2010-12-29 | GSE15449 | GEO

SDF-1 induced transcriptional changes in human cord blood CD34+ cells

Project description:We have employed whole genome microarray expression profiling to identify genes differentially expressed in cord blood enriched CD34+ cells(>95%) after a short-term exposure to the chemokine stromal cell-derived factor-1 (SDF-1). SDF-1 induced gene expressions of cord blood enriched CD34+ cells were measured at 4 hours. Four biological replicates were performed for each treatment group.

2011-01-01 | E-GEOD-20891 | biostudies-arrayexpress

Global gene expression profiles of MT knockout and wild-type mice in the condition of doxorubicin-induced cardiomyopathy

Project description:The present study was designed using MT knockout mice in concert with genomic approaches to explore the possible molecular and cellular mechanisms involved in the protective effects of MT against DOX cardiotoxicity. MT-M-bM-^EM- /M-bM-^EM-! null (MT-/-) mice and corresponding wild-type mice (MT+/+) were administrated with a single dose of DOX (15 mg/kg, i.p.) or an equal volume of saline. Animals were sacrificed on the 4th day after DOX administration and samples were collected for further analyses. Global gene expression profiles of cardiac mRNA from two genotype mice revealed that 381 characteristically MT-responsive genes were identified between MT+/+ mice and MT-/- mice in response to DOX, including fos, ucp3, car3, atf3, map3k6, etc.. Functional analysis implied MAPK signaling pathway, p53 signaling pathway, Jak-STAT signaling pathway, PPAR signaling pathway, Wnt signaling pathway, etc. might be involved to mediate the protection of DOX cardiomyopathy by MT. Results from the present study not only validated the previously reported possible mechanisms of MT protection against DOX toxicity, but also provided new clues into the molecular mechanisms involved in this process. Male MT+/+ & MT-/- mice (6-8 weeks old) were randomly assigned to treatment or control groups and administrated with a single dose of DOX (15 mg/kg, i.p.) or an equal volume of normal saline solution (NS) respectively. Animals were sacrificed on the 4th day after DOX injection, and samples were collected for further microarray analyses.

2013-08-10 | E-GEOD-23598 | biostudies-arrayexpress

Targeted disruption of BMAL1 in the peripheral reproductive axis results in infertility in female mice

Project description:The product of the Bmal1 locus is an essential component of the circadian clock that plays important roles in various aspects of reproductive biology,and when disrupted results in infertility. In an effort to establish the identity of the tissue specific clock that is responsible for this infertility, we used the steroidogenic factor-1 (Sf1) promoter to drive Cre-mediated recombination and genetically delete Bmal1 within cells of the reproductive axis. We show that Bmal1 within the reproductive axis of females is essential for normal fertility through its role in maintaining implantation, but is not required for normal estrous cycling. At the root of this biology appears to be a defect in the ovaries, including regulation of ovarian lipid biosynthetic or metabolic processes and their roles in maintaining progesterone synthesis. This conclusion is based upon three observations. First, that deletion of Bmal1 within the reproductive axis reducesleads to affected transcripts in steroidogenic pathways for the LH receptor , and lowers progesterone levels. Second, that progesterone supplementation of these conditional mutants rescues implantation. Third, transplantation of wild type ovaries into Bmal1 reproductive axis mutants rescues fertility. Our study demonstrates the significance of ovarian Bmal1 as an overriding influence in experimental models of infertility. A time series was performed in time-mated C57Bl/6J mice to identiy oscillating transcripts. During the peak and trough of the majority of transcripts (ZT0 and ZT12) samples from Bmal1fx/fx Sf1Cre mice and control litermates as well and global Bmal1 nulls were also analyzed. The tissue types (ovary, pituitary) are not comparable.

2014-10-01 | E-GEOD-48758 | biostudies-arrayexpress

Comparison of gene expression between Human umbilical vein endothelial cells and Human liver sinusoidal endothelial cells

Project description:To identify leukocyte adhesion receptors which differentially regulate recruitment in human liver sinusoidal endothelial cells compared to a protoptypic venular endothelium Gene expression was measured in four groups Group 1: cultured human liver sinusoidal endothelial cells (HSEC) Group 2: cultured human umbilical vein endothelial cells (HUVEC) Group3: Interferon gamma and tumour necrosisfactor alpha treated HSEC and Group 4: Interferon gamma and tumour necrosisfactor alpha treated HUVEC. Two replicates were used for each group.

2016-10-24 | E-GEOD-78020 | biostudies-arrayexpress

Conditional keratinocyte-specific ADAM17 knockout in mice alters skin homeostasis

Project description:This study investigates the role of ADAM17 (a disintegrin and metalloproteinase 17) in skin homeostasis. Here, we show that mice lacking ADAM17 in keratinocytes have a normal epidermal barrier and skin architecture at birth, but develop pronounced defects in epidermal barrier integrity soon after birth and chronic dermatitis as adults. The dysregulated expression of epidermal differentiation proteins becomes evident 2 days after birth, followed by transepidermal water loss and inflammatory immune cell infiltration. Our results identify a previously unappreciated critical role of the ADAM17/EGFR signaling axis in maintaining the homeostasis of the postnatal epidermal barrier. The genome-wide effects of ADAM17 deficiency were analyzed using Agilent Whole Mouse Genome microarrays. Conditional keratinocyte-specific ADAM17 knockout mice were generated by crossing Adam17flox/flox mice with keratin-14-Cre (Krt14-Cre) transgenic mice. Adam17flox/+Krt14-Cre mice were mated with Adam17flox/flox mice to generate pups of Adam17flox/flox Krt14-Cre positive (cKO) and Krt14-Cre negative (wild-type) control littermates. The genetic background was a mix of 129Sv and C57BL/6. As material, back skin tissue biopsies (postnatal day 10) from n = 2 wild-type skin and n = 2 ADAM17 epidermal KO skin (matched WT-cKO pairs from two different litters) were used in this study.

2012-06-20 | E-GEOD-38830 | biostudies-arrayexpress

Inducible Gata1 Suppression Expands Erythro-Megakaryocytic Progenitors from Embryonic Stem Cells

Project description:Embryonic stem (ES) and induced pluripotent stem (iPS) cells represent a potential source of megakaryocytes and platelets for transfusion therapies. However, most current ES/iPS cell differentiation protocols are limited by low yields of hematopoietic progeny. Mutations in the mouse and human genes encoding transcription factor GATA1 cause accumulation of proliferating, developmentally arrested megakaryocytes. To exploit this clinical observation, we engineered wildtype (WT) murine ES cells to express doxycycline (dox)-regulated Gata1 short hairpin (sh) RNAs. In vitro differentiation with dox and thrombopoietin (Tpo) resulted in approximately 1013-fold expansion of immature hematopoietic progenitors. Upon dox withdrawal with multilineage cytokines, GATA1 expression was restored and the cells differentiated into erythroblasts and megakaryocytes. With Tpo alone, dox-deprived progenitors formed mainly mature megakaryocytes that generated functional platelets in vivo. Our findings provide a novel, readily reproducible strategy to expand ES-cell derived megakaryocyte-erythroid progenitors and direct their differentiation into megakaryocytes producing functional platelets in clinically relevant numbers. 3 classes of samples were compared 1) fetal liver derived megkaryocytes 2) G1ME (Gata1â megakaryocyte-erythroid) 3) G1ME2 (engineered wildtype (WT) murine ES cells to express doxycycline (dox)-regulated Gata1 short hairpin (sh) RNAs)

2015-12-09 | E-GEOD-66479 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data