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Book ; Online ; Thesis: Long non-coding RNAs involved in myeloid cell differentiation and macrophage activation

Aznaourova, Marina [Verfasser] / Schulte, Leon [Akademischer Betreuer]

2021

Author's details	Marina Aznaourova ; Betreuer: Leon Schulte
Keywords	Medizin, Gesundheit ; Medicine, Health
Subject code	sg610
Language	English
Publisher	Philipps-Universität Marburg
Publishing place	Marburg
Document type	Book ; Online ; Thesis
Database	Digital theses on the web

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Article: Disease-Causing Mutations and Rearrangements in Long Non-coding RNA Gene Loci.

Aznaourova, Marina / Schmerer, Nils / Schmeck, Bernd / Schulte, Leon N

Frontiers in genetics

2020 Volume 11, Page(s) 527484

Abstract: The classic understanding of molecular disease-mechanisms is largely based on protein-centric models. During the past decade however, genetic studies have identified numerous disease-loci in the human genome that do not encode proteins. Such non-coding ... ...

Abstract	The classic understanding of molecular disease-mechanisms is largely based on protein-centric models. During the past decade however, genetic studies have identified numerous disease-loci in the human genome that do not encode proteins. Such non-coding DNA variants increasingly gain attention in diagnostics and personalized medicine. Of particular interest are long non-coding RNA (lncRNA) genes, which generate transcripts longer than 200 nucleotides that are not translated into proteins. While most of the estimated ~20,000 lncRNAs currently remain of unknown function, a growing number of genetic studies link lncRNA gene aberrations with the development of human diseases, including diabetes, AIDS, inflammatory bowel disease, or cancer. This suggests that the protein-centric view of human diseases does not capture the full complexity of molecular patho-mechanisms, with important consequences for molecular diagnostics and therapy. This review illustrates well-documented lncRNA gene aberrations causatively linked to human diseases and discusses potential lessons for molecular disease models, diagnostics, and therapy.
Language	English
Publishing date	2020-11-30
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2606823-0
ISSN	1664-8021
ISSN	1664-8021
DOI	10.3389/fgene.2020.527484
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Biofilm formation on human immune cells is a multicellular predation strategy of Vibrio cholerae.

Vidakovic, Lucia / Mikhaleva, Sofya / Jeckel, Hannah / Nisnevich, Valerya / Strenger, Kerstin / Neuhaus, Konstantin / Raveendran, Keerthana / Ben-Moshe, Noa Bossel / Aznaourova, Marina / Nosho, Kazuki / Drescher, Antje / Schmeck, Bernd / Schulte, Leon N / Persat, Alexandre / Avraham, Roi / Drescher, Knut

Cell

2023 Volume 186, Issue 12, Page(s) 2690–2704.e20

Abstract: Biofilm formation is generally recognized as a bacterial defense mechanism against environmental threats, including antibiotics, bacteriophages, and leukocytes of the human immune system. Here, we show that for the human pathogen Vibrio cholerae, biofilm ...

Abstract	Biofilm formation is generally recognized as a bacterial defense mechanism against environmental threats, including antibiotics, bacteriophages, and leukocytes of the human immune system. Here, we show that for the human pathogen Vibrio cholerae, biofilm formation is not only a protective trait but also an aggressive trait to collectively predate different immune cells. We find that V. cholerae forms biofilms on the eukaryotic cell surface using an extracellular matrix comprising primarily mannose-sensitive hemagglutinin pili, toxin-coregulated pili, and the secreted colonization factor TcpF, which differs from the matrix composition of biofilms on other surfaces. These biofilms encase immune cells and establish a high local concentration of a secreted hemolysin to kill the immune cells before the biofilms disperse in a c-di-GMP-dependent manner. Together, these results uncover how bacteria employ biofilm formation as a multicellular strategy to invert the typical relationship between human immune cells as the hunters and bacteria as the hunted.
MeSH term(s)	Animals ; Humans ; Vibrio cholerae/metabolism ; Predatory Behavior ; Biofilms ; Fimbriae, Bacterial ; Bacterial Proteins/metabolism ; Gene Expression Regulation, Bacterial
Chemical Substances	Bacterial Proteins
Language	English
Publishing date	2023-06-08
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	187009-9
ISSN	1097-4172 ; 0092-8674
ISSN (online)	1097-4172
ISSN	0092-8674
DOI	10.1016/j.cell.2023.05.008
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Zs.A 1167: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (1.OG) ab Jg. 2022: Lesesaal (EG)
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Article ; Online: Cas9-mediated excision of proximal DNaseI/H3K4me3 signatures confers robust silencing of microRNA and long non-coding RNA genes.

Janga, Harshavardhan / Aznaourova, Marina / Boldt, Fabian / Damm, Katrin / Grünweller, Arnold / Schulte, Leon N

PloS one

2018 Volume 13, Issue 2, Page(s) e0193066

Abstract: CRISPR/Cas9-based approaches have greatly facilitated targeted genomic deletions. Contrary to coding genes however, which can be functionally knocked out by frame-shift mutagenesis, non-coding RNA (ncRNA) gene knockouts have remained challenging. Here we ...

Abstract	CRISPR/Cas9-based approaches have greatly facilitated targeted genomic deletions. Contrary to coding genes however, which can be functionally knocked out by frame-shift mutagenesis, non-coding RNA (ncRNA) gene knockouts have remained challenging. Here we present a universal ncRNA knockout approach guided by epigenetic hallmarks, which enables robust gene silencing even in provisionally annotated gene loci. We build on previous work reporting the presence of overlapping histone H3 lysine 4 tri-methylation (H3K4me3) and DNaseI hypersensitivity sites around the transcriptional start sites of most genes. We demonstrate that excision of this gene-proximal signature leads to loss of microRNA and lincRNA transcription and reveals ncRNA phenotypes. Exemplarily we demonstrate silencing of the constitutively transcribed MALAT1 lincRNA gene as well as of the inducible miR-146a and miR-155 genes in human monocytes. Our results validate a role of miR-146a and miR-155 in negative feedback control of the activity of inflammation master-regulator NFκB and suggest that cell-cycle control is a unique feature of miR-155. We suggest that our epigenetically guided CRISPR approach may improve existing ncRNA knockout strategies and contribute to the development of high-confidence ncRNA phenotyping applications.
MeSH term(s)	Blotting, Northern ; Clustered Regularly Interspaced Short Palindromic Repeats/genetics ; Deoxyribonuclease I/genetics ; Deoxyribonuclease I/metabolism ; Flow Cytometry ; Gene Expression Regulation/genetics ; Gene Knockout Techniques/methods ; Gene Silencing ; Histones/genetics ; Humans ; MicroRNAs/genetics ; Monocytes/metabolism ; RNA, Long Noncoding/genetics ; Real-Time Polymerase Chain Reaction
Chemical Substances	Histones ; MicroRNAs ; RNA, Long Noncoding ; Deoxyribonuclease I (EC 3.1.21.1)
Language	English
Publishing date	2018
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ISSN	1932-6203
ISSN (online)	1932-6203
DOI	10.1371/journal.pone.0193066
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Single-cell RNA sequencing uncovers the nuclear decoy lincRNA PIRAT as a regulator of systemic monocyte immunity during COVID-19.

Aznaourova, Marina / Schmerer, Nils / Janga, Harshavardhan / Zhang, Zhenhua / Pauck, Kim / Bushe, Judith / Volkers, Sarah M / Wendisch, Daniel / Georg, Philipp / Ntini, Evgenia / Aillaud, Michelle / Gündisch, Margrit / Mack, Elisabeth / Skevaki, Chrysanthi / Keller, Christian / Bauer, Christian / Bertrams, Wilhelm / Marsico, Annalisa / Nist, Andrea /

Stiewe, Thorsten / Gruber, Achim D / Ruppert, Clemens / Li, Yang / Garn, Holger / Sander, Leif E / Schmeck, Bernd / Schulte, Leon N

Proceedings of the National Academy of Sciences of the United States of America

2022 Volume 119, Issue 36, Page(s) e2120680119

Abstract: The systemic immune response to viral infection is shaped by master transcription factors, such as NF-κB, STAT1, or PU.1. Although long noncoding RNAs (lncRNAs) have been suggested as important regulators of transcription factor activity, their ... ...

Abstract	The systemic immune response to viral infection is shaped by master transcription factors, such as NF-κB, STAT1, or PU.1. Although long noncoding RNAs (lncRNAs) have been suggested as important regulators of transcription factor activity, their contributions to the systemic immunopathologies observed during SARS-CoV-2 infection have remained unknown. Here, we employed a targeted single-cell RNA sequencing approach to reveal lncRNAs differentially expressed in blood leukocytes during severe COVID-19. Our results uncover the lncRNA PIRAT (PU.1-induced regulator of alarmin transcription) as a major PU.1 feedback-regulator in monocytes, governing the production of the alarmins S100A8/A9, key drivers of COVID-19 pathogenesis. Knockout and transgene expression, combined with chromatin-occupancy profiling, characterized PIRAT as a nuclear decoy RNA, keeping PU.1 from binding to alarmin promoters and promoting its binding to pseudogenes in naïve monocytes. NF-κB-dependent PIRAT down-regulation during COVID-19 consequently releases a transcriptional brake, fueling alarmin production. Alarmin expression is additionally enhanced by the up-regulation of the lncRNA LUCAT1, which promotes NF-κB-dependent gene expression at the expense of targets of the JAK-STAT pathway. Our results suggest a major role of nuclear noncoding RNA networks in systemic antiviral responses to SARS-CoV-2 in humans.
MeSH term(s)	Alarmins/genetics ; COVID-19/genetics ; COVID-19/immunology ; Gene Expression Regulation ; Humans ; Janus Kinases/genetics ; Monocytes/immunology ; NF-kappa B/genetics ; RNA, Long Noncoding/genetics ; RNA, Long Noncoding/metabolism ; RNA-Seq ; SARS-CoV-2/immunology ; STAT Transcription Factors/genetics ; Signal Transduction/genetics ; Single-Cell Analysis
Chemical Substances	Alarmins ; NF-kappa B ; RNA, Long Noncoding ; STAT Transcription Factors ; Janus Kinases (EC 2.7.10.2)
Language	English
Publishing date	2022-08-23
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	209104-5
ISSN	1091-6490 ; 0027-8424
ISSN (online)	1091-6490
ISSN	0027-8424
DOI	10.1073/pnas.2120680119
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Article ; Online: Insulin Resistance in Macrophages Alters Their Metabolism and Promotes an M2-Like Phenotype.

Ieronymaki, Eleftheria / Theodorakis, Emmanouel M / Lyroni, Konstantina / Vergadi, Eleni / Lagoudaki, Eleni / Al-Qahtani, Ahmed / Aznaourova, Marina / Neofotistou-Themeli, Elpida / Eliopoulos, Aristides G / Vaporidi, Katerina / Tsatsanis, Christos

Journal of immunology (Baltimore, Md. : 1950)

2019 Volume 202, Issue 6, Page(s) 1786–1797

Abstract: Obesity and insulin resistance influences metabolic processes, but whether it affects macrophage metabolism is not known. In this study, we demonstrate that chronic exposure of macrophages to insulin either in culture or in vivo in diet-induced, glucose- ... ...

Abstract	Obesity and insulin resistance influences metabolic processes, but whether it affects macrophage metabolism is not known. In this study, we demonstrate that chronic exposure of macrophages to insulin either in culture or in vivo in diet-induced, glucose-intolerant mice rendered them resistant to insulin signals marked by failure to induce Akt2 phosphorylation. Similarly, macrophages lacking Akt2 or IGF1 receptor were also resistant to insulin signals. Insulin-resistant macrophages had increased basal mTORC1 activity, possessed an M2-like phenotype, and reduced LPS responses. Moreover, they exhibited increased glycolysis and increased expression of key glycolytic enzymes. Inhibition of mTORC1 reversed the M2-like phenotype and suppressed glycolysis in insulin-resistant macrophages. In the context of polymicrobial sepsis, mice harboring insulin-resistant macrophages exhibited reduced sepsis-induced lung injury. Thus, macrophages obtain resistance to insulin characterized by increased glycolysis and a unique M2-like phenotype, termed M-insulin resistant, which accounts for obesity-related changes in macrophage responses and a state of trained immunity.
MeSH term(s)	Animals ; Inflammation/immunology ; Inflammation/metabolism ; Insulin Resistance/physiology ; Macrophage Activation/physiology ; Macrophages/immunology ; Macrophages/metabolism ; Male ; Mice ; Mice, Inbred C57BL ; Obesity/complications ; Phenotype
Language	English
Publishing date	2019-02-04
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	3056-9
ISSN	1550-6606 ; 0022-1767 ; 1048-3233 ; 1047-7381
ISSN (online)	1550-6606
ISSN	0022-1767 ; 1048-3233 ; 1047-7381
DOI	10.4049/jimmunol.1800065
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Article ; Online: Noncoding RNA

Aznaourova, Marina / Janga, Harshavardhan / Sefried, Stephanie / Kaufmann, Andreas / Dorna, Jens / Volkers, Sarah M / Georg, Philipp / Lechner, Marcus / Hoppe, Judith / Dökel, Simon / Schmerer, Nils / Gruber, Achim D / Linne, Uwe / Bauer, Stefan / Sander, Leif E / Schmeck, Bernd / Schulte, Leon N

Proceedings of the National Academy of Sciences of the United States of America

2020 Volume 117, Issue 16, Page(s) 9042–9053

Abstract: RNA has been proposed as an important scaffolding factor in the nucleus, aiding protein complex assembly in the dense intracellular milieu. Architectural contributions of RNA to cytosolic signaling pathways, however, remain largely unknown. Here, we ... ...

Abstract	RNA has been proposed as an important scaffolding factor in the nucleus, aiding protein complex assembly in the dense intracellular milieu. Architectural contributions of RNA to cytosolic signaling pathways, however, remain largely unknown. Here, we devised a multidimensional gradient approach, which systematically locates RNA components within cellular protein networks. Among a subset of noncoding RNAs (ncRNAs) cosedimenting with the ubiquitin-proteasome system, our approach unveiled ncRNA
MeSH term(s)	Adaptor Proteins, Vesicular Transport/metabolism ; Adult ; Aged ; Blood Buffy Coat/cytology ; Bronchoalveolar Lavage Fluid/immunology ; Cell Cycle Proteins/metabolism ; Female ; Gene Expression Regulation/immunology ; Gene Knockdown Techniques ; Humans ; Interferon Regulatory Factor-3/metabolism ; Interferon Type I/blood ; Interferon Type I/genetics ; Interferon Type I/immunology ; Macrophages ; Male ; Membrane Transport Proteins/metabolism ; Middle Aged ; Phosphorylation/genetics ; Primary Cell Culture ; Protein Stability ; Protein-Serine-Threonine Kinases/metabolism ; RNA, Untranslated/blood ; RNA, Untranslated/genetics ; RNA, Untranslated/metabolism ; RNA-Seq ; Respiratory Tract Infections/blood ; Respiratory Tract Infections/immunology ; Respiratory Tract Infections/microbiology ; Signal Transduction/genetics ; Signal Transduction/immunology ; Toll-Like Receptor 4/metabolism ; Young Adult
Chemical Substances	Adaptor Proteins, Vesicular Transport ; Cell Cycle Proteins ; IRF3 protein, human ; Interferon Regulatory Factor-3 ; Interferon Type I ; Membrane Transport Proteins ; OPTN protein, human ; RNA, Untranslated ; TICAM1 protein, human ; TLR4 protein, human ; Toll-Like Receptor 4 ; Protein-Serine-Threonine Kinases (EC 2.7.11.1) ; TBK1 protein, human (EC 2.7.11.1)
Language	English
Publishing date	2020-04-02
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	209104-5
ISSN	1091-6490 ; 0027-8424
ISSN (online)	1091-6490
ISSN	0027-8424
DOI	10.1073/pnas.1920393117
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Article ; Online: Middle east respiratory syndrome corona virus spike glycoprotein suppresses macrophage responses via DPP4-mediated induction of IRAK-M and PPARγ.

Al-Qahtani, Ahmed A / Lyroni, Konstantina / Aznaourova, Marina / Tseliou, Melpomeni / Al-Anazi, Mashael R / Al-Ahdal, Mohammed N / Alkahtani, Saad / Sourvinos, George / Tsatsanis, Christos

Oncotarget

2017 Volume 8, Issue 6, Page(s) 9053–9066

Abstract: Middle East Respiratory Syndrome Corona Virus (MERS-CoV) is transmitted via the respiratory tract and causes severe Acute Respiratory Distress Syndrome by infecting lung epithelial cells and macrophages. Macrophages can readily recognize the virus and ... ...

Abstract	Middle East Respiratory Syndrome Corona Virus (MERS-CoV) is transmitted via the respiratory tract and causes severe Acute Respiratory Distress Syndrome by infecting lung epithelial cells and macrophages. Macrophages can readily recognize the virus and eliminate it. MERS-CoV infects cells via its Spike (S) glycoprotein that binds on Dipeptidyl-Peptidase 4 (DPP4) receptor present on macrophages. Whether this Spike/DPP4 association affects macrophage responses remains unknown. Herein we demonstrated that infection of macrophages with lentiviral particles pseudotyped with MERS-CoV S glycoprotein results in suppression of macrophage responses since it reduced the capacity of macrophages to produce TNFα and IL-6 in naive and LPS-activated THP-1 macrophages and augmented LPS-induced production of the immunosuppressive cytokine IL-10. MERS-CoV S glycoprotein induced the expression of the negative regulator of TLR signaling IRAK-M as well as of the transcriptional repressor PPARγ. Inhibition of DPP4 by its inhibitor sitagliptin or siRNA abrogated the effects of MERS-CoV S glycoprotein on IRAK-M, PPARγ and IL-10, confirming that its immunosuppressive effects were mediated by DPP4 receptor. The effect was observed both in THP-1 macrophages and human primary peripheral blood monocytes. These findings support a DPP4-mediated suppressive action of MERS-CoV in macrophages and suggest a potential target for effective elimination of its pathogenicity.
Keywords	covid19
Language	English
Publishing date	2017-02-07
Publishing country	United States
Document type	Journal Article
ZDB-ID	2560162-3
ISSN	1949-2553 ; 1949-2553
ISSN (online)	1949-2553
ISSN	1949-2553
DOI	10.18632/oncotarget.14754
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Single cell RNA-seq uncovers the nuclear decoy lincRNA PIRAT as a regulator of systemic monocyte immunity during COVID-19

Aznaourova, Marina / Schmerer, Nils / Janga, Harshavardhan / Zhang, Zhenhua / Pauck, Kim / Hoppe, Judith / Volkers, Sarah M / Wendisch, Daniel / Georg, Philipp / Guendisch, Margrit / Mack, Elisabeth / Skevaki, Chrysanthi / Keller, Christian / Bauer, Christian / Bertrams, Wilhelm / Nist, Andrea / Stiewe, Thorsten / Gruber, Achim D / Ruppert, Clemens /

Li, Yang / Garn, Holger / Sander, Leif E / Schmeck, Bernd / Schulte, Leon N

bioRxiv

Abstract: The systemic immune response to viral infection is shaped by master transcription factors such as NFκB or PU.1. Although long non-coding RNAs (lncRNAs) have been suggested as important regulators of transcription factor activity, their contributions to ... ...

Abstract	The systemic immune response to viral infection is shaped by master transcription factors such as NFκB or PU.1. Although long non-coding RNAs (lncRNAs) have been suggested as important regulators of transcription factor activity, their contributions to the systemic immunopathologies observed during SARS-CoV-2 infection have remained unknown. Here, we employed a targeted single-cell RNA-seq approach to reveal lncRNAs differentially expressed in blood leukocytes during severe COVID-19. Our results uncover the lncRNA PIRAT as a major PU.1 feedback-regulator in monocytes, governing the production of the alarmins S100A8/A9 - key drivers of COVID-19 pathogenesis. Knockout and transgene expression, combined with chromatin-occupancy profiling characterized PIRAT as a nuclear decoy RNA, diverting the PU.1 transcription factor from alarmin promoters to dead-end pseudogenes in naive monocytes. NFκB-dependent PIRAT down-regulation during COVID-19 consequently releases a transcriptional brake, fueling alarmin production. Our results suggest a major role of nuclear noncoding RNA circuits in systemic antiviral responses to SARS-CoV-2 in humans.
Keywords	covid19
Language	English
Publishing date	2021-11-05
Publisher	Cold Spring Harbor Laboratory
Document type	Article ; Online
DOI	10.1101/2021.11.05.467458
Database	COVID19

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