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Article: Sexually dimorphic renal expression of

Jankowski, Jakub / Lee, Hye Kyung / Liu, Chengyu / Wilflingseder, Julia / Hennighausen, Lothar

bioRxiv : the preprint server for biology

2024

Abstract: Transcription enhancers are genomic sequences regulating common and tissue-specific genes and their disruption can contribute to human disease development and progression. ...

Abstract	Transcription enhancers are genomic sequences regulating common and tissue-specific genes and their disruption can contribute to human disease development and progression.
Language	English
Publishing date	2024-03-04
Publishing country	United States
Document type	Preprint
DOI	10.1101/2024.02.29.582831
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Article ; Online: JAK inhibitors dampen activation of interferon-activated transcriptomes and the SARS-CoV-2 receptor ACE2 in human renal proximal tubules.

Jankowski, Jakub / Lee, Hye Kyung / Wilflingseder, Julia / Hennighausen, Lothar

iScience

2021 Volume 24, Issue 8, Page(s) 102928

Abstract: SARS-CoV-2 infections initiate cytokine storms and activate genetic programs leading to progressive hyperinflammation in multiple organs of patients with COVID-19. While it is known that COVID-19 impacts kidney function, leading to increased mortality, ... ...

Abstract	SARS-CoV-2 infections initiate cytokine storms and activate genetic programs leading to progressive hyperinflammation in multiple organs of patients with COVID-19. While it is known that COVID-19 impacts kidney function, leading to increased mortality, cytokine response of renal epithelium has not been studied in detail. Here, we report on the genetic programs activated in human primary proximal tubule (HPPT) cells by interferons and their suppression by ruxolitinib, a Janus kinase (JAK) inhibitor used in COVID-19 treatment. Integration of our data with those from patients with acute kidney injury and COVID-19, as well as other tissues, permitted the identification of kidney-specific interferon responses. Additionally, we investigated the regulation of the recently discovered isoform (dACE2) of the angiotensin-converting enzyme 2 (ACE2), the SARS-CoV-2 receptor. Using ChIP-seq, we identified candidate interferon-activated enhancers controlling the
Language	English
Publishing date	2021-07-30
Publishing country	United States
Document type	Journal Article
ISSN	2589-0042
ISSN (online)	2589-0042
DOI	10.1016/j.isci.2021.102928
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Article: Interferon-regulated genetic programs and JAK/STAT pathway activate the intronic promoter of the short ACE2 isoform in renal proximal tubules.

Jankowski, Jakub / Lee, Hye Kyung / Wilflingseder, Julia / Hennighausen, Lothar

bioRxiv : the preprint server for biology

2021

Abstract: Recently, a short, interferon-inducible isoform of Angiotensin-Converting Enzyme 2 (ACE2), dACE2 was identified. ACE2 is a SARS-Cov-2 receptor and changes in its renal expression have been linked to several human nephropathies. These changes were never ... ...

Abstract	Recently, a short, interferon-inducible isoform of Angiotensin-Converting Enzyme 2 (ACE2), dACE2 was identified. ACE2 is a SARS-Cov-2 receptor and changes in its renal expression have been linked to several human nephropathies. These changes were never analyzed in context of
Language	English
Publishing date	2021-01-19
Publishing country	United States
Document type	Preprint
DOI	10.1101/2021.01.15.426908
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Article ; Online: Interferon-regulated genetic programs and JAK/STAT pathway activate the intronic promoter of the short ACE2 isoform in renal proximal tubules

Jankowski, Jakub / Lee, Hye Kyung / Wilflingseder, Julia / Hennighausen, Lothar

bioRxiv

Abstract: Summary: Recently, a short, interferon-inducible isoform of Angiotensin-Converting Enzyme 2 (ACE2), dACE2 was identified. ACE2 is a SARS-Cov-2 receptor and changes in its renal expression have been linked to several human nephropathies. These changes ... ...

Abstract	Summary: Recently, a short, interferon-inducible isoform of Angiotensin-Converting Enzyme 2 (ACE2), dACE2 was identified. ACE2 is a SARS-Cov-2 receptor and changes in its renal expression have been linked to several human nephropathies. These changes were never analyzed in context of dACE2, as its expression was not investigated in the kidney. We used Human Primary Proximal Tubule (HPPT) cells to show genome-wide gene expression patterns after cytokine stimulation, with emphasis on the ACE2/dACE2 locus. Putative regulatory elements controlling dACE2 expression were identified using ChIP-seq and RNA-seq. qRT-PCR differentiating between ACE2 and dACE2 revealed 300- and 600-fold upregulation of dACE2 by IFNα and IFNβ, respectively, while full length ACE2 expression was almost unchanged. JAK inhibitor ruxolitinib ablated STAT1 and dACE2 expression after interferon treatment. Finally, with RNA-seq, we identified a set of genes, largely immune-related, induced by cytokine treatment. These gene expression profiles provide new insights into cytokine response of proximal tubule cells.
Keywords	covid19
Language	English
Publishing date	2021-01-19
Publisher	Cold Spring Harbor Laboratory
Document type	Article ; Online
DOI	10.1101/2021.01.15.426908
Database	COVID19

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Article ; Online: Enhancer and super-enhancer dynamics in repair after ischemic acute kidney injury.

Wilflingseder, Julia / Willi, Michaela / Lee, Hye Kyung / Olauson, Hannes / Jankowski, Jakub / Ichimura, Takaharu / Erben, Reinhold / Valerius, M Todd / Hennighausen, Lothar / Bonventre, Joseph V

Nature communications

2020 Volume 11, Issue 1, Page(s) 3383

Abstract: The endogenous repair process can result in recovery after acute kidney injury (AKI) with adaptive proliferation of tubular epithelial cells, but repair can also lead to fibrosis and progressive kidney disease. There is currently limited knowledge about ... ...

Abstract	The endogenous repair process can result in recovery after acute kidney injury (AKI) with adaptive proliferation of tubular epithelial cells, but repair can also lead to fibrosis and progressive kidney disease. There is currently limited knowledge about transcriptional regulators regulating these repair programs. Herein we establish the enhancer and super-enhancer landscape after AKI by ChIP-seq in uninjured and repairing kidneys on day two after ischemia reperfusion injury (IRI). We identify key transcription factors including HNF4A, GR, STAT3 and STAT5, which show specific binding at enhancer and super-enhancer sites, revealing enhancer dynamics and transcriptional changes during kidney repair. Loss of bromodomain-containing protein 4 function before IRI leads to impaired recovery after AKI and increased mortality. Our comprehensive analysis of epigenetic changes after kidney injury in vivo has the potential to identify targets for therapeutic intervention. Importantly, our data also call attention to potential caveats involved in use of BET inhibitors in patients at risk for AKI.
MeSH term(s)	Acute Kidney Injury/genetics ; Acute Kidney Injury/metabolism ; Amino Acid Motifs ; Animals ; Binding Sites ; Cell Proliferation ; Enhancer Elements, Genetic ; Epigenesis, Genetic ; Fibrosis ; Hepatocyte Nuclear Factor 4/metabolism ; Kidney/metabolism ; Kidney/pathology ; Kidney Tubules/cytology ; Male ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; Nuclear Proteins ; Receptors, Glucocorticoid/metabolism ; Regulatory Elements, Transcriptional ; Reperfusion Injury/metabolism ; STAT3 Transcription Factor/metabolism ; STAT5 Transcription Factor/metabolism ; Signal Transduction ; Transcription Factors ; Transcription, Genetic
Chemical Substances	Brd4 protein, mouse ; Hepatocyte Nuclear Factor 4 ; Hnf4a protein, mouse ; Nuclear Proteins ; Receptors, Glucocorticoid ; STAT3 Transcription Factor ; STAT5 Transcription Factor ; Stat3 protein, mouse ; Transcription Factors
Language	English
Publishing date	2020-07-07
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, N.I.H., Intramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2553671-0
ISSN	2041-1723 ; 2041-1723
ISSN (online)	2041-1723
ISSN	2041-1723
DOI	10.1038/s41467-020-17205-5
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Article ; Online: miR-182-5p Inhibition Ameliorates Ischemic Acute Kidney Injury.

Wilflingseder, Julia / Jelencsics, Kíra / Bergmeister, Helga / Sunzenauer, Judith / Regele, Heinz / Eskandary, Farsad / Reindl-Schwaighofer, Roman / Kainz, Alexander / Oberbauer, Rainer

The American journal of pathology

2017 Volume 187, Issue 1, Page(s) 70–79

Abstract: Acute kidney injury (AKI) remains a major clinical event with high mortality rates. We previously identified renal miR-182 as the main driver of post-transplantation AKI. Therefore, we tested the causal inference of miR-182 by inhibiting its renal ... ...

Abstract	Acute kidney injury (AKI) remains a major clinical event with high mortality rates. We previously identified renal miR-182 as the main driver of post-transplantation AKI. Therefore, we tested the causal inference of miR-182 by inhibiting its renal expression in vivo. In 45 rats AKI was induced by right nephrectomy and contralateral clamping of the renal pedicle for 40 minutes. Systemically administered antisense oligonucleotide (ASO) inhibited miR-182 in the kidneys up to 96 hours. The maximum creatinine elevation was on day 2 after injury (mg/dL; median and interquartile range): ASO 2.5mg/kg: 1.9 (1.3; 3.2), ASO 25mg/kg: 2.8 (0.7; 5.0), mismatch oligonucleotide (MM) 25mg/kg: 5.7 (5,0; 5.8), saline: 4.4 (3.5; 5.8) (P = 0.016, analysis of variance). Blinded semiquantitative histologic evaluation of renal biopsies showed better preserved morphology in both ASO groups than saline- and MM-treated kidneys (median and interquartile range of overall injury scores): ASO both concentrations 1 (1, 1), saline 3 (3, 3) and MM 3 (3, 3) (P< 0.001, analysis of variance). ASO facilitated cell proliferation, metabolism, and angiogenesis on a genome-wide level. ASO when applied in normothermic kidney machine perfusion reduced renal miR-182 expression by more than two magnitudes. In summary, we showed that in vivo inhibition of miR-182 by ASO improved kidney function and morphology after AKI. This technique may be applicable to reduce the high rate of AKI in the human renal transplantation setting.
MeSH term(s)	Acute Kidney Injury/genetics ; Acute Kidney Injury/pathology ; Animals ; Biopsy ; Cells, Cultured ; Disease Progression ; Gene Expression Regulation/drug effects ; Humans ; Ischemia/genetics ; Ischemia/pathology ; Kidney/blood supply ; Kidney/drug effects ; Kidney/metabolism ; Kidney/pathology ; Male ; Mice, Inbred C57BL ; MicroRNAs/antagonists & inhibitors ; MicroRNAs/metabolism ; Oligonucleotides, Antisense/pharmacology ; Rats, Sprague-Dawley ; Reperfusion Injury/genetics ; Reperfusion Injury/pathology ; Reproducibility of Results ; Sus scrofa
Chemical Substances	MIRN182 microRNA, rat ; MicroRNAs ; Oligonucleotides, Antisense
Language	English
Publishing date	2017-01
Publishing country	United States
Document type	Journal Article
ZDB-ID	2943-9
ISSN	1525-2191 ; 0002-9440
ISSN (online)	1525-2191
ISSN	0002-9440
DOI	10.1016/j.ajpath.2016.09.011
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Article ; Online: Indian Hedgehog release from TNF-activated renal epithelia drives local and remote organ fibrosis.

O'Sullivan, Eoin D / Mylonas, Katie J / Xin, Cuiyan / Baird, David P / Carvalho, Cyril / Docherty, Marie-Helena / Campbell, Ross / Matchett, Kylie P / Waddell, Scott H / Walker, Alexander D / Gallagher, Kevin M / Jia, Siyang / Leung, Steve / Laird, Alexander / Wilflingseder, Julia / Willi, Michaela / Reck, Maximilian / Finnie, Sarah / Pisco, Angela /

Gordon-Keylock, Sabrina / Medvinsky, Alexander / Boulter, Luke / Henderson, Neil C / Kirschner, Kristina / Chandra, Tamir / Conway, Bryan R / Hughes, Jeremy / Denby, Laura / Bonventre, Joseph V / Ferenbach, David A

Science translational medicine

2023 Volume 15, Issue 698, Page(s) eabn0736

Abstract: Progressive fibrosis is a feature of aging and chronic tissue injury in multiple organs, including the kidney and heart. Glioma-associated oncogene 1 expressing ( ... ...

Abstract	Progressive fibrosis is a feature of aging and chronic tissue injury in multiple organs, including the kidney and heart. Glioma-associated oncogene 1 expressing (Gli1
MeSH term(s)	Animals ; Humans ; Mice ; Fibrosis ; Hedgehog Proteins/metabolism ; Inflammation ; NF-kappa B ; Renal Insufficiency, Chronic ; Tumor Necrosis Factors ; Zinc Finger Protein GLI1
Chemical Substances	Hedgehog Proteins ; NF-kappa B ; Tumor Necrosis Factors ; Zinc Finger Protein GLI1 ; IHH protein, human ; ihh protein, mouse
Language	English
Publishing date	2023-05-31
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2518854-9
ISSN	1946-6242 ; 1946-6234
ISSN (online)	1946-6242
ISSN	1946-6234
DOI	10.1126/scitranslmed.abn0736
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Article ; Online: Hemoglobin variability after renal transplantation is associated with mortality.

Kainz, Alexander / Wilflingseder, Julia / Függer, Reinhold / Kramar, Reinhard / Oberbauer, Rainer

Transplant international : official journal of the European Society for Organ Transplantation

2012 Volume 25, Issue 3, Page(s) 323–327

Abstract: Anemia is a common problem after renal transplantation. Therefore, the patients are treated with erythropoietin stimulating agents (ESAs). The varying response to treatment contributes to hemoglobin variability, which might be associated with mortality. ... ...

Abstract	Anemia is a common problem after renal transplantation. Therefore, the patients are treated with erythropoietin stimulating agents (ESAs). The varying response to treatment contributes to hemoglobin variability, which might be associated with mortality. We conducted a retrospective cohort study of first kidney allograft recipients between 1990 and 2008 represented in the Austrian Transplant Registry. We included 1441 patients of whom 683 received ESAs at any time after transplantation. Cox regression with cubic splines and linear estimates and the purposeful selection algorithm of covariables were used. The measure of variability was the moving standard deviation computed at three monthly intervals for the entire graft life. The hazard ratio (HR) of mortality and graft loss in the spline models increased with hemoglobin variability. The linear HR for mortality was 2.35 (95% confidence interval 1.75-3.17, P<0.001) and functional graft loss 2.45 (1.76-3.40, P<0.001). In an adjusted Cox model (ESA use, hemoglobin, age, diabetes, days on dialysis, eGFR, biopsy confirmed acute rejection and year of transplantation), hemoglobin variability was associated with mortality (HR: 2.11; 1.51-2.94; P<0.001). No association with functional graft loss could be detected (HR: 1.34; 0.93-1.93; P=0.121). These findings suggest that hemoglobin variability is associated with mortality of renal allograft recipients.
MeSH term(s)	Adult ; Anemia/blood ; Anemia/drug therapy ; Anemia/etiology ; Biomarkers/metabolism ; Cohort Studies ; Female ; Hematinics/therapeutic use ; Hemoglobins/metabolism ; Humans ; Kidney Transplantation/mortality ; Male ; Middle Aged ; Postoperative Complications/blood ; Postoperative Complications/drug therapy ; Primary Graft Dysfunction/blood ; Primary Graft Dysfunction/etiology ; Proportional Hazards Models ; Registries ; Retrospective Studies ; Treatment Outcome
Chemical Substances	Biomarkers ; Hematinics ; Hemoglobins
Language	English
Publishing date	2012-02-01
Publishing country	England
Document type	Evaluation Study ; Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	639435-8
ISSN	1432-2277 ; 0934-0874
ISSN (online)	1432-2277
ISSN	0934-0874
DOI	10.1111/j.1432-2277.2012.01428.x
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Article ; Online: Orphan nuclear receptor COUP-TFII enhances myofibroblast glycolysis leading to kidney fibrosis.

Li, Li / Galichon, Pierre / Xiao, Xiaoyan / Figueroa-Ramirez, Ana C / Tamayo, Diana / Lee, Jake J-K / Kalocsay, Marian / Gonzalez-Sanchez, David / Chancay, Maria S / McCracken, Kyle W / Lee, Nathan N / Ichimura, Takaharu / Mori, Yutaro / Valerius, M Todd / Wilflingseder, Julia / Lemos, Dario R / Edelman, Elazer R / Bonventre, Joseph V

EMBO reports

2021 Volume 22, Issue 6, Page(s) e51169

Abstract: Recent studies demonstrate that metabolic disturbance, such as augmented glycolysis, contributes to fibrosis. The molecular regulation of this metabolic perturbation in fibrosis, however, has been elusive. COUP-TFII (also known as NR2F2) is an important ... ...

Abstract	Recent studies demonstrate that metabolic disturbance, such as augmented glycolysis, contributes to fibrosis. The molecular regulation of this metabolic perturbation in fibrosis, however, has been elusive. COUP-TFII (also known as NR2F2) is an important regulator of glucose and lipid metabolism. Its contribution to organ fibrosis is undefined. Here, we found increased COUP-TFII expression in myofibroblasts in human fibrotic kidneys, lungs, kidney organoids, and mouse kidneys after injury. Genetic ablation of COUP-TFII in mice resulted in attenuation of injury-induced kidney fibrosis. A non-biased proteomic study revealed the suppression of fatty acid oxidation and the enhancement of glycolysis pathways in COUP-TFII overexpressing fibroblasts. Overexpression of COUP-TFII in fibroblasts also induced production of alpha-smooth muscle actin (αSMA) and collagen 1. Knockout of COUP-TFII decreased glycolysis and collagen 1 levels in fibroblasts. Chip-qPCR revealed the binding of COUP-TFII on the promoter of PGC1α. Overexpression of COUP-TFII reduced the cellular level of PGC1α. Targeting COUP-TFII serves as a novel treatment approach for mitigating fibrosis in chronic kidney disease and potentially fibrosis in other organs.
MeSH term(s)	Animals ; COUP Transcription Factor II/genetics ; COUP Transcription Factor II/metabolism ; Fibrosis ; Glycolysis/genetics ; Kidney ; Mice ; Mice, Knockout ; Myofibroblasts ; Orphan Nuclear Receptors/metabolism ; Proteomics
Chemical Substances	COUP Transcription Factor II ; Nr2f2 protein, mouse ; Orphan Nuclear Receptors
Language	English
Publishing date	2021-05-25
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2020896-0
ISSN	1469-3178 ; 1469-221X
ISSN (online)	1469-3178
ISSN	1469-221X
DOI	10.15252/embr.202051169
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Zs.A 5433: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (2.OG) ab Jg. 2022: Lesesaal (EG)
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Article ; Online: Interleukin-1

Lemos, Dario R / McMurdo, Michael / Karaca, Gamze / Wilflingseder, Julia / Leaf, Irina A / Gupta, Navin / Miyoshi, Tomoya / Susa, Koichiro / Johnson, Bryce G / Soliman, Kirolous / Wang, Guanghai / Morizane, Ryuji / Bonventre, Joseph V / Duffield, Jeremy S

Journal of the American Society of Nephrology : JASN

2018 Volume 29, Issue 6, Page(s) 1690–1705

Abstract: ... ...

Abstract	Background
MeSH term(s)	Acute Kidney Injury/metabolism ; Acute Kidney Injury/pathology ; Animals ; Autophagy/drug effects ; Azepines/pharmacology ; Carrier Proteins/metabolism ; Cell Proliferation/drug effects ; Cells, Cultured ; Disease Progression ; Extracellular Matrix/metabolism ; Fibrosis ; Glycolysis/drug effects ; Humans ; Interleukin-1 Receptor-Associated Kinases/antagonists & inhibitors ; Interleukin-1 Receptor-Associated Kinases/metabolism ; Interleukin-1beta/pharmacology ; Kidney/cytology ; Kidney/pathology ; Kidney Tubules, Proximal/pathology ; Male ; Membrane Proteins/metabolism ; Mice ; Organoids ; Proto-Oncogene Proteins c-myc/antagonists & inhibitors ; Proto-Oncogene Proteins c-myc/genetics ; Proto-Oncogene Proteins c-myc/metabolism ; Renal Insufficiency, Chronic/metabolism ; Renal Insufficiency, Chronic/pathology ; Sequestosome-1 Protein/genetics ; Sequestosome-1 Protein/metabolism ; Signal Transduction ; Stromal Cells/metabolism ; Thyroid Hormones/metabolism ; Triazoles/pharmacology ; Thyroid Hormone-Binding Proteins
Chemical Substances	(+)-JQ1 compound ; Azepines ; Carrier Proteins ; IL1B protein, human ; Interleukin-1beta ; MYC protein, human ; Membrane Proteins ; Myc protein, mouse ; Proto-Oncogene Proteins c-myc ; SQSTM1 protein, human ; Sequestosome-1 Protein ; Thyroid Hormones ; Triazoles ; IRAK4 protein, human (EC 2.7.11.1) ; Interleukin-1 Receptor-Associated Kinases (EC 2.7.11.1) ; Irak4 protein, mouse (EC 2.7.11.1)
Language	English
Publishing date	2018-05-08
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	1085942-1
ISSN	1533-3450 ; 1046-6673
ISSN (online)	1533-3450
ISSN	1046-6673
DOI	10.1681/ASN.2017121283
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