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Transcriptome analysis reveals hub genes and Ihh and KLF9 axis in the endometrial restoration in IUA mice

ABSTRACT: Transcriptome analysis reveals hub genes and Ihh and KLF9 axis in the endometrial restoration in IUA mice

PROVIDER: PRJNA898615 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR22199100_1.fastq.gz	Fastqsanger.gz
	SRR22199100_2.fastq.gz	Fastqsanger.gz
	SRR22199101_1.fastq.gz	Fastqsanger.gz
	SRR22199101_2.fastq.gz	Fastqsanger.gz
	SRR22199102_1.fastq.gz	Fastqsanger.gz

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Transcriptome analysis reveals hub genes and Ihh and KLF9 axis in the endometrial restoration in IUA mice

Project description:To investigate the molecular mechanism during the restoration of mouse endometrium by CRCs transplantation, uterine horns were collected from the mice of CRC cells- transplanted, injury and sham operated groups at 7 days after surgery for RNAsequencing (RNA-seq). We then performed gene expression profiling analysis using data obtained from RNA-seq of three groups mice.

2022-12-28 | GSE217365 | GEO

Klf9 is essential for cardiac mitochondrial homeostasis

Project description:Mitochondrial dynamics and mitophagy are intimately linked physiological processes that are essential for cardiac homeostasis. Here we show that cardiac Klf9 is dysregulated in human and rodent cardiomyopathy. Young adult global Klf9-knockout mice displayed hypertrophic cardiomyopathy that was characterized by depressed systolic function, increased left ventricular mass and pulmonary congestion. Klf9 knockout led to mitochondrial disarray and fragmentation in cardiomyocytes. Biochemical analysis confirmed that mitochondrial respiratory function was impaired in Klf9-knockout cardiomyocytes, with reduced myocardial ATP levels and elevated ROS. Furthermore, cardiac-specific Klf9-deficient mice phenocopied global Klf9-knockout mice, suggesting that cardiac Klf9 is essential for mitochondrial homeostasis and heart function. Moreover, cardiac Klf9 deficiency inhibited mitophagy induced by angiotensin II (ANGII), thereby leading to accumulation of dysfunctional mitochondria and acceleration of heart failure in mice in response to ANGII treatment. In contrast, cardiac-specific Klf9 transgene improved cardiac systolic function via promoting mitophagy in mice in response to ANGII treatment. Molecular mechanism studies indicated that Klf9 knockout decreased the expression of PGC-1α and its target genes involved in mitochondrial energy metabolism. Moreover, Klf9 controlled the expression of Mfn2 by directly binding to its promoter region, thereby regulating mitochondrial dynamics and mitophagy. Finally, we performed Mfn2 rescue experiments in Klf9-CKO mice and found that AAV-mediated Mfn2 rescue in heart improved cardiac mitochondrial and systolic function in Klf9-CKO mice treated with or without ANGII. Thus, Klf9 integrates cardiac energy metabolism, mitochondrial dynamics and mitophagy. Modulating Klf9 activity may have therapeutic potential in the treatment of heart failure.

2024-10-03 | GSE278326 | GEO

Global changes in gene expression in primary keratinocytes after KLF9 overexpression

Project description:To identify putative target genes of the transcription factor Klf9 in primary keratinocytes we over-expressed Klf9 in these cells using a lentiviral delivery system. We detected several hundred genes that show differential expression levels following ectopic Klf9 expression including several genes that are involved in proliferation and cell cycle control. These results allow insights into the mechanisms by which Klf9 regulates proliferation in primary keratinocytes. Primary human neonatal foreskin keratinocytes were infected with equal viral titers of a GFP and KLF9 expression construct, respectively. Cells were harvested 2,4 and 7 days after infection and total RNA was used to perform whole genome microarray analysis.

2012-07-30 | E-GEOD-36014 | biostudies-arrayexpress

Transcription profiling of jejunums from wild type and Klf9-/- mice to investigate the involvement of Klf9 in small intestine crypt-villus cell renewal and lineage determination.

Project description:Kruppel-like factor 9 (Klf9), a zinc-finger transcription factor, is implicated in the control of cell proliferation, cell differentiation and cell fate in brain and uterus. Using Klf9 null mutant mice, we have investigated the involvement of Klf9 in small intestine crypt-villus cell renewal and lineage determination. We report the predominant expression of Klf9 gene in small intestine smooth muscle (muscularis externa). Jejunums null for Klf9 have shorter villi, reduced crypt stem/transit cell proliferation, and altered lineage determination as indicated by decreased and increased numbers of Goblet and Paneth cells, respectively. A stimulatory role for Klf9 in villus cell migration was demonstrated by BrdU labeling. Results suggest that Klf9 controls the elaboration, from small intestine smooth muscle, of molecular mediator(s) of crypt cell proliferation and lineage determination, and of villus cell migration. Experiment Overall Design: Total RNA was extracted in parallel from the jejunums of five WT and five Klf9-/- male mice (PND 30) using TRIzol reagent (Invitrogen, Carlsbad, CA). Conversion of each RNA preparation to corresponding fragmented cRNA. Fifteen ug of each cRNA was hybridized for 16 hours to an Affymetrix mouse 430A GeneChip. Ten GeneChips (each corresponding to a single animal) were hybridized, washed and scanned in parallel. Following the wash, signal amplification, and signal detection steps, GeneChips were scanned (Agilent GeneArray laser scanner) and the resultant images quantified using Affymetrix MAS 5.0 software.

2007-11-15 | E-GEOD-6443 | biostudies-arrayexpress

A Krüppel-like factor 9 (Klf9) regulated network in HEC-1-A endometrial carcinoma cells

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Endometrial transcriptomic profiles in patients with severe IUA and normal control

Project description:Intrauterine adhesion (IUA) is characterized by endometrial fibrosis with partial or complete uterine cavity obliteration. IUA patients often undergo amenorrhea/ hypomenorrhea, abdominal pain, infertility, early pregnancy loss or severe placental complications. In this work, endometria samples were collected from severe IUA and control patients. RNA-seq was performed to identify differences between IUA and normal control and investigate the mechanisms of IUA development.

2023-06-12 | GSE224093 | GEO

Transcriptomes comparisons of Dhh KO, Ihh KO and Dhh/Ihh DKO ovaries

Project description:The goal of the microarray analysis is to determine the redundant and distinct roles of Dhh and Ihh in ovarian functions

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Transcriptomes comparisons of Dhh KO, Ihh KO and Dhh/Ihh DKO ovaries

Project description:Transcriptomes comparisons of Dhh KO, Ihh KO and Dhh/Ihh DKO ovaries

| PRJNA432169 | ENA

Global changes in gene expression in primary keratinocytes after KLF9 overexpression

2012-07-31 | GSE36014 | GEO

Identification of Klf9-regulated genes in HT22 tissue culture cells [RNA-Seq]

Project description:Krueppel-like factor 9 (Klf9) is a DNA-binding transcription factor that has been implicated in neuronal development and regeneration. We used mouse hippocampus-derived HT22 cell line to identify genes differentially regulated by forced Klf9 expression. We stably transfected HT22 cells with pCDNA6:TR (encoding the Tet repressor) and pCDNA6:TO-Klf9 (encoding Klf9 downstream of the Tet operator), allowing doxycycline(dox)-inducible expression of Klf9. We chose a stably transfected clone with baseline Klf9 mRNA level similar to that of untransfected HT22 cells (parent line) and approximately 10-fold induction after dox treatment. We conducted RNA-seq on stably transfected HT22 cells treated with or without dox for 8 hours; we also conducted RNA-seq on parent cells subjected to the same dox treatment to separate nonspecific effects of dox from the effects of forced Klf9 expression. Analysis of RNA-seq data found 217 gene repressed and 21 upregulated by forced Klf9 expression (FDR-adjusted p<.005; because fold changes were small we used a stringent p value cutoff to ensure that we were studying genes likely to be bona fide targets), showing that Klf9 functions primarily as a transcriptional repressor. Gene ontology analysis showed that Klf9-repressed genes were enriched in cytoskeletal and Wnt signaling-related genes.

2019-09-19 | GSE87093 | GEO

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