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Loss of proximal tubular Kruppel-like factor 15 (KLF15) exacerbates kidney injury through loss of fatty acid oxidation

ABSTRACT: Loss of proximal tubular Kruppel-like factor 15 (KLF15) exacerbates kidney injury through loss of fatty acid oxidation

PROVIDER: PRJNA631162 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR11732437.fastq.gz	Fastqsanger.gz
	SRR11732438.fastq.gz	Fastqsanger.gz
	SRR11732439.fastq.gz	Fastqsanger.gz
	SRR11732440.fastq.gz	Fastqsanger.gz
	SRR11732441.fastq.gz	Fastqsanger.gz

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Loss of proximal tubular Kruppel-like factor 15 (KLF15) exacerbates kidney injury through loss of fatty acid oxidation

Project description:KLF15 has a critical role in other kidney cell types, but its role in mediating proximal tubular (PT) fatty acid oxidation (FAO) in AKI has not been determined. PT-specific KLF15 knockdown (Klf15PTKO) and control Klf15fl/fl mice were treated with multiple low doses of the PT-specific DNA-damaging agent aristolochic acid I (AAI) and RNA-sequencing of kidney cortex undertaken. Klf15PTKO exhibited worse kidney injury than Klf15fl/fl mice after AAI treatment. Immune system and integrin signaling pathways were significantly upregulated in Klf15PTKO versus Klf15fl/fl mice. Metabolic pathways, specifically FAO, were significantly downregulated in Klf15PTKO versus Klf15fl/fl mice, including PPARalpha signaling.

2023-04-28 | GSE150098 | GEO

Transcription profiling of mouse livers and quadriceps muscles of Kruppel-like factor 15 (KLF15) null mutants after an overnight fast to provide insight into the role of KLF15 in gluconeogenesis

Project description:We used microarray analysis to identify differences in gene expression levels, in liver and in quadriceps skeletal muscle, between 18h (overnight) fasted WT control and Kruppel-like factor 15 (KLF15)-null mice. Experiment Overall Design: Liver and skeletal muscle (quadriceps) tissues were isolated from 4-5 month old, 18h-fasted WT and KLF15-null female mice for RNA extraction and hybridization on Affymetrix microarrays.

2007-11-07 | E-GEOD-7137 | biostudies-arrayexpress

Loss of proximal tubular Kruppel-like factor 6 (KLF6) is protective against AKI and CKD

Project description:Loss of proximal tubular Kruppel-like factor 6 (KLF6) is protective against AKI and CKD

| PRJNA633101 | ENA

Endothelial KLF15/VASN axis inhibits angiogenesis via activation of Notch1 signaling [ChIP-Seq]

Project description:Kruppel like factors (KLFs) are a subfamily of zinc finger proteins. As one of the family members, KLF15 can specifically bind to GC rich sequences on the promoter, thereby exerting transcriptional regulatory effects. Here we found that KLF15 negatively regulates angiogenesis in endothelial cells. KLF15 induces an increase in vasorin (VASN) expression, thereby activating the Notch signaling pathway and leading to a decrease in angiogenesis. These findings point to an KLF15/VASN axis as critical determinants of Notch signaling activation.

2025-05-24 | GSE287265 | GEO

Endothelial KLF15/VASN axis inhibits angiogenesis via activation of Notch1 signaling [ATAC-Seq]

2025-05-24 | GSE287264 | GEO

KLF15

Project description:KLF15

| PRJNA301030 | ENA

Expression data from 18h-fasted WT versus KLF15-null mice: liver and quadriceps skeletal muscle

2007-04-02 | GSE7137 | GEO

KLF15 Cistromes Reveal a Hepatocyte Pathway Governing Plasma Corticosteroid Transport and Systemic Inflammation

Project description:Circulating corticosteroids orchestrate stress adaptation, including inhibition of inflammation. While pathways governing corticosteroid biosynthesis and intracellular signaling are understood, less is known about mechanisms controlling plasma corticosteroid transport. Here, we show hepatocyte KLF15 (Kruppel-like factor 15) controls plasma corticosteroid transport and inflammatory responses through direct transcriptional activation of Serpina6, which encodes corticosteroid binding globulin (CBG). Klf15-deficient mice have profoundly low CBG, reduced plasma corticosteroid binding capacity, and heightened mortality during inflammatory stress. These defects are completely rescued by reconstituting CBG, supporting that KLF15 works primarily through CBG to control plasma corticosterone homeostasis. To understand transcriptional mechanisms, we generated the first KLF15 cistromes using newly engineered Klf153xFLAG mice. Unexpectedly, liver KLF15 is predominantly promoter-enriched, including Serpina6, where it binds a palindromic GC-rich motif, opens chromatin, and transactivates genes with minimal associated gene repression. Overall, we provide new mechanistic insight into KLF15 function and identify a hepatocyte-intrinsic transcriptional module that potently regulates systemic corticosteroid transport and inflammation.

2021-12-28 | GSE166083 | GEO

Loss of proximal tubular transcription factor Kruppel-like factor 15 exacerbates kidney injury through loss of fatty acid oxidation.

Project description:Loss of fatty acid β-oxidation (FAO) in the proximal tubule is a critical mediator of acute kidney injury and eventual fibrosis. However, transcriptional mediators of FAO in proximal tubule injury remain understudied. Krüppel-like factor 15 (KLF15), a highly enriched zinc-finger transcription factor in the proximal tubule, was significantly reduced in proximal tubule cells after aristolochic acid I (AAI) treatment, a proximal tubule-specific injury model. Proximal tubule specific knockout of Klf15 exacerbated proximal tubule injury and kidney function decline compared to control mice during the active phase of AAI treatment, and after ischemia-reperfusion injury. Furthermore, along with worsening proximal tubule injury and kidney function decline, knockout mice exhibited increased kidney fibrosis as compared to control mice during the remodeling phase after AAI treatment. RNA-sequencing of kidney cortex demonstrated increased transcripts involved in immune system and integrin signaling pathways and decreased transcripts encompassing metabolic pathways, specifically FAO, and PPARα signaling, in knockout versus control mice after AAI treatment. In silico and experimental chromatin immunoprecipitation studies collectively demonstrated that KLF15 occupied the promoter region of key FAO genes, CPT1A and ACAA2, in close proximity to transcription factor PPARα binding sites. While the loss of Klf15 reduced the expression of Cpt1a and Acaa2 and led to compromised FAO, induction of KLF15 partially rescued loss of FAO in AAI-treated cells. Klf15, Ppara, Cpt1a, and Acaa2 expression was also decreased in other mouse kidney injury models. Tubulointerstitial KLF15 independently correlated with eGFR, PPARA and CPT1A appearance in expression arrays from human kidney biopsies. Thus, proximal tubule-specific loss of Klf15 exacerbates acute kidney injury and fibrosis, likely due to loss of interaction with PPARα leading to loss of FAO gene transcription.

| S-EPMC8608748 | biostudies-literature

Effect of Klf15 on gene expression in Mrps5 null heart at 14 weeks after Mrps5 gene knockout

Project description:To understand the molecular mechanisms by which Klf15 overexpression rescues the Mrps5 loss of function phenotype in the heart. We conducted RNA sequencing to profile the transcriptomes of Mrps5cKO mice infected with AAV9-Klf15 or control AAV9-Luci.

2023-02-14 | GSE200999 | GEO

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