Role of endothelial microRNA 155 on capillary leakage in systemic inflammation
Background Capillary leakage is a key contributor to the pathological host response to infections. The underlying mechanisms remain incompletely understood, and the role of microRNAs (MIR) has not been investigated in detail. We hypothesized that specific MIRs might be regulated directly in the endo...
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| Published in | Critical care (London, England) Vol. 25; no. 1; pp. 76 - 12 |
|---|---|
| Main Authors | , , , , , , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
London
BioMed Central
22.02.2021
BioMed Central Ltd BMC |
| Subjects | |
| Online Access | Get full text |
| ISSN | 1364-8535 1466-609X 1364-8535 1466-609X 1366-609X |
| DOI | 10.1186/s13054-021-03500-0 |
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| Abstract | Background
Capillary leakage is a key contributor to the pathological host response to infections. The underlying mechanisms remain incompletely understood, and the role of microRNAs (MIR) has not been investigated in detail. We hypothesized that specific MIRs might be regulated directly in the endothelium thereby contributing to vascular leakage.
Methods
SmallRNA sequencing of endotoxemic murine pulmonary endothelial cells (ECs) was done to detect regulated vascular MIRs. In vivo models: transgenic zebrafish (flk1:mCherry/l-fabp:eGFP-DPB), knockout/wildtype mouse (B6.Cg-Mir155tm1.1Rsky/J); disease models: LPS 17.5 mg/kgBW and cecal ligation and puncture (CLP); in vitro models: stimulated human umbilical vein EC (HUVECs), transendothelial electrical resistance.
Results
Endothelial MIR155 was identified as a promising candidate in endotoxemic murine pulmonary ECs (25 × upregulation). Experimental overexpression in a transgenic zebrafish line and in HUVECs was sufficient to induce spontaneous vascular leakage. To the contrary, genetic MIR155 reduction protects against permeability both in vitro and in endotoxemia in vivo in MIR155 heterozygote knockout mice thereby improving survival by 40%. A tight junction protein, Claudin-1, was down-regulated both in endotoxemia and by experimental MIR155 overexpression. Translationally, MIR155 was detectable at high levels in bronchoalveolar fluid of patients with ARDS compared to healthy human subjects.
Conclusions
We found that MIR155 is upregulated in the endothelium in mouse and men as part of a systemic inflammatory response and might contribute to the pathophysiology of vascular leakage in a Claudin-1-dependent manner. Future studies have to clarify whether MIR155 could be a potential therapeutic target. |
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| AbstractList | Capillary leakage is a key contributor to the pathological host response to infections. The underlying mechanisms remain incompletely understood, and the role of microRNAs (MIR) has not been investigated in detail. We hypothesized that specific MIRs might be regulated directly in the endothelium thereby contributing to vascular leakage.
SmallRNA sequencing of endotoxemic murine pulmonary endothelial cells (ECs) was done to detect regulated vascular MIRs. In vivo models: transgenic zebrafish (flk1:mCherry/l-fabp:eGFP-DPB), knockout/wildtype mouse (B6.Cg-Mir155tm1.1Rsky/J); disease models: LPS 17.5 mg/kgBW and cecal ligation and puncture (CLP); in vitro models: stimulated human umbilical vein EC (HUVECs), transendothelial electrical resistance.
Endothelial MIR155 was identified as a promising candidate in endotoxemic murine pulmonary ECs (25 × upregulation). Experimental overexpression in a transgenic zebrafish line and in HUVECs was sufficient to induce spontaneous vascular leakage. To the contrary, genetic MIR155 reduction protects against permeability both in vitro and in endotoxemia in vivo in MIR155 heterozygote knockout mice thereby improving survival by 40%. A tight junction protein, Claudin-1, was down-regulated both in endotoxemia and by experimental MIR155 overexpression. Translationally, MIR155 was detectable at high levels in bronchoalveolar fluid of patients with ARDS compared to healthy human subjects.
We found that MIR155 is upregulated in the endothelium in mouse and men as part of a systemic inflammatory response and might contribute to the pathophysiology of vascular leakage in a Claudin-1-dependent manner. Future studies have to clarify whether MIR155 could be a potential therapeutic target. Capillary leakage is a key contributor to the pathological host response to infections. The underlying mechanisms remain incompletely understood, and the role of microRNAs (MIR) has not been investigated in detail. We hypothesized that specific MIRs might be regulated directly in the endothelium thereby contributing to vascular leakage. SmallRNA sequencing of endotoxemic murine pulmonary endothelial cells (ECs) was done to detect regulated vascular MIRs. In vivo models: transgenic zebrafish (flk1:mCherry/l-fabp:eGFP-DPB), knockout/wildtype mouse (B6.Cg-Mir155tm1.1Rsky/J); disease models: LPS 17.5 mg/kgBW and cecal ligation and puncture (CLP); in vitro models: stimulated human umbilical vein EC (HUVECs), transendothelial electrical resistance. Endothelial MIR155 was identified as a promising candidate in endotoxemic murine pulmonary ECs (25 x upregulation). Experimental overexpression in a transgenic zebrafish line and in HUVECs was sufficient to induce spontaneous vascular leakage. To the contrary, genetic MIR155 reduction protects against permeability both in vitro and in endotoxemia in vivo in MIR155 heterozygote knockout mice thereby improving survival by 40%. A tight junction protein, Claudin-1, was down-regulated both in endotoxemia and by experimental MIR155 overexpression. Translationally, MIR155 was detectable at high levels in bronchoalveolar fluid of patients with ARDS compared to healthy human subjects. We found that MIR155 is upregulated in the endothelium in mouse and men as part of a systemic inflammatory response and might contribute to the pathophysiology of vascular leakage in a Claudin-1-dependent manner. Future studies have to clarify whether MIR155 could be a potential therapeutic target. Background Capillary leakage is a key contributor to the pathological host response to infections. The underlying mechanisms remain incompletely understood, and the role of microRNAs (MIR) has not been investigated in detail. We hypothesized that specific MIRs might be regulated directly in the endothelium thereby contributing to vascular leakage. Methods SmallRNA sequencing of endotoxemic murine pulmonary endothelial cells (ECs) was done to detect regulated vascular MIRs. In vivo models: transgenic zebrafish (flk1:mCherry/l-fabp:eGFP-DPB), knockout/wildtype mouse (B6.Cg-Mir155tm1.1Rsky/J); disease models: LPS 17.5 mg/kgBW and cecal ligation and puncture (CLP); in vitro models: stimulated human umbilical vein EC (HUVECs), transendothelial electrical resistance. Results Endothelial MIR155 was identified as a promising candidate in endotoxemic murine pulmonary ECs (25 x upregulation). Experimental overexpression in a transgenic zebrafish line and in HUVECs was sufficient to induce spontaneous vascular leakage. To the contrary, genetic MIR155 reduction protects against permeability both in vitro and in endotoxemia in vivo in MIR155 heterozygote knockout mice thereby improving survival by 40%. A tight junction protein, Claudin-1, was down-regulated both in endotoxemia and by experimental MIR155 overexpression. Translationally, MIR155 was detectable at high levels in bronchoalveolar fluid of patients with ARDS compared to healthy human subjects. Conclusions We found that MIR155 is upregulated in the endothelium in mouse and men as part of a systemic inflammatory response and might contribute to the pathophysiology of vascular leakage in a Claudin-1-dependent manner. Future studies have to clarify whether MIR155 could be a potential therapeutic target. Keywords: Tight junctions, Respiratory distress syndrome, MicroRNAs, Endothelium, Sepsis Capillary leakage is a key contributor to the pathological host response to infections. The underlying mechanisms remain incompletely understood, and the role of microRNAs (MIR) has not been investigated in detail. We hypothesized that specific MIRs might be regulated directly in the endothelium thereby contributing to vascular leakage.BACKGROUNDCapillary leakage is a key contributor to the pathological host response to infections. The underlying mechanisms remain incompletely understood, and the role of microRNAs (MIR) has not been investigated in detail. We hypothesized that specific MIRs might be regulated directly in the endothelium thereby contributing to vascular leakage.SmallRNA sequencing of endotoxemic murine pulmonary endothelial cells (ECs) was done to detect regulated vascular MIRs. In vivo models: transgenic zebrafish (flk1:mCherry/l-fabp:eGFP-DPB), knockout/wildtype mouse (B6.Cg-Mir155tm1.1Rsky/J); disease models: LPS 17.5 mg/kgBW and cecal ligation and puncture (CLP); in vitro models: stimulated human umbilical vein EC (HUVECs), transendothelial electrical resistance.METHODSSmallRNA sequencing of endotoxemic murine pulmonary endothelial cells (ECs) was done to detect regulated vascular MIRs. In vivo models: transgenic zebrafish (flk1:mCherry/l-fabp:eGFP-DPB), knockout/wildtype mouse (B6.Cg-Mir155tm1.1Rsky/J); disease models: LPS 17.5 mg/kgBW and cecal ligation and puncture (CLP); in vitro models: stimulated human umbilical vein EC (HUVECs), transendothelial electrical resistance.Endothelial MIR155 was identified as a promising candidate in endotoxemic murine pulmonary ECs (25 × upregulation). Experimental overexpression in a transgenic zebrafish line and in HUVECs was sufficient to induce spontaneous vascular leakage. To the contrary, genetic MIR155 reduction protects against permeability both in vitro and in endotoxemia in vivo in MIR155 heterozygote knockout mice thereby improving survival by 40%. A tight junction protein, Claudin-1, was down-regulated both in endotoxemia and by experimental MIR155 overexpression. Translationally, MIR155 was detectable at high levels in bronchoalveolar fluid of patients with ARDS compared to healthy human subjects.RESULTSEndothelial MIR155 was identified as a promising candidate in endotoxemic murine pulmonary ECs (25 × upregulation). Experimental overexpression in a transgenic zebrafish line and in HUVECs was sufficient to induce spontaneous vascular leakage. To the contrary, genetic MIR155 reduction protects against permeability both in vitro and in endotoxemia in vivo in MIR155 heterozygote knockout mice thereby improving survival by 40%. A tight junction protein, Claudin-1, was down-regulated both in endotoxemia and by experimental MIR155 overexpression. Translationally, MIR155 was detectable at high levels in bronchoalveolar fluid of patients with ARDS compared to healthy human subjects.We found that MIR155 is upregulated in the endothelium in mouse and men as part of a systemic inflammatory response and might contribute to the pathophysiology of vascular leakage in a Claudin-1-dependent manner. Future studies have to clarify whether MIR155 could be a potential therapeutic target.CONCLUSIONSWe found that MIR155 is upregulated in the endothelium in mouse and men as part of a systemic inflammatory response and might contribute to the pathophysiology of vascular leakage in a Claudin-1-dependent manner. Future studies have to clarify whether MIR155 could be a potential therapeutic target. Background Capillary leakage is a key contributor to the pathological host response to infections. The underlying mechanisms remain incompletely understood, and the role of microRNAs (MIR) has not been investigated in detail. We hypothesized that specific MIRs might be regulated directly in the endothelium thereby contributing to vascular leakage. Methods SmallRNA sequencing of endotoxemic murine pulmonary endothelial cells (ECs) was done to detect regulated vascular MIRs. In vivo models: transgenic zebrafish (flk1:mCherry/l-fabp:eGFP-DPB), knockout/wildtype mouse (B6.Cg-Mir155tm1.1Rsky/J); disease models: LPS 17.5 mg/kgBW and cecal ligation and puncture (CLP); in vitro models: stimulated human umbilical vein EC (HUVECs), transendothelial electrical resistance. Results Endothelial MIR155 was identified as a promising candidate in endotoxemic murine pulmonary ECs (25 × upregulation). Experimental overexpression in a transgenic zebrafish line and in HUVECs was sufficient to induce spontaneous vascular leakage. To the contrary, genetic MIR155 reduction protects against permeability both in vitro and in endotoxemia in vivo in MIR155 heterozygote knockout mice thereby improving survival by 40%. A tight junction protein, Claudin-1, was down-regulated both in endotoxemia and by experimental MIR155 overexpression. Translationally, MIR155 was detectable at high levels in bronchoalveolar fluid of patients with ARDS compared to healthy human subjects. Conclusions We found that MIR155 is upregulated in the endothelium in mouse and men as part of a systemic inflammatory response and might contribute to the pathophysiology of vascular leakage in a Claudin-1-dependent manner. Future studies have to clarify whether MIR155 could be a potential therapeutic target. Abstract Background Capillary leakage is a key contributor to the pathological host response to infections. The underlying mechanisms remain incompletely understood, and the role of microRNAs (MIR) has not been investigated in detail. We hypothesized that specific MIRs might be regulated directly in the endothelium thereby contributing to vascular leakage. Methods SmallRNA sequencing of endotoxemic murine pulmonary endothelial cells (ECs) was done to detect regulated vascular MIRs. In vivo models: transgenic zebrafish (flk1:mCherry/l-fabp:eGFP-DPB), knockout/wildtype mouse (B6.Cg-Mir155tm1.1Rsky/J); disease models: LPS 17.5 mg/kgBW and cecal ligation and puncture (CLP); in vitro models: stimulated human umbilical vein EC (HUVECs), transendothelial electrical resistance. Results Endothelial MIR155 was identified as a promising candidate in endotoxemic murine pulmonary ECs (25 × upregulation). Experimental overexpression in a transgenic zebrafish line and in HUVECs was sufficient to induce spontaneous vascular leakage. To the contrary, genetic MIR155 reduction protects against permeability both in vitro and in endotoxemia in vivo in MIR155 heterozygote knockout mice thereby improving survival by 40%. A tight junction protein, Claudin-1, was down-regulated both in endotoxemia and by experimental MIR155 overexpression. Translationally, MIR155 was detectable at high levels in bronchoalveolar fluid of patients with ARDS compared to healthy human subjects. Conclusions We found that MIR155 is upregulated in the endothelium in mouse and men as part of a systemic inflammatory response and might contribute to the pathophysiology of vascular leakage in a Claudin-1-dependent manner. Future studies have to clarify whether MIR155 could be a potential therapeutic target. Background Capillary leakage is a key contributor to the pathological host response to infections. The underlying mechanisms remain incompletely understood, and the role of microRNAs (MIR) has not been investigated in detail. We hypothesized that specific MIRs might be regulated directly in the endothelium thereby contributing to vascular leakage. Methods SmallRNA sequencing of endotoxemic murine pulmonary endothelial cells (ECs) was done to detect regulated vascular MIRs. In vivo models: transgenic zebrafish (flk1:mCherry/l-fabp:eGFP-DPB), knockout/wildtype mouse (B6.Cg-Mir155tm1.1Rsky/J); disease models: LPS 17.5 mg/kgBW and cecal ligation and puncture (CLP); in vitro models: stimulated human umbilical vein EC (HUVECs), transendothelial electrical resistance. Results Endothelial MIR155 was identified as a promising candidate in endotoxemic murine pulmonary ECs (25 × upregulation). Experimental overexpression in a transgenic zebrafish line and in HUVECs was sufficient to induce spontaneous vascular leakage. To the contrary, genetic MIR155 reduction protects against permeability both in vitro and in endotoxemia in vivo in MIR155 heterozygote knockout mice thereby improving survival by 40%. A tight junction protein, Claudin-1, was down-regulated both in endotoxemia and by experimental MIR155 overexpression. Translationally, MIR155 was detectable at high levels in bronchoalveolar fluid of patients with ARDS compared to healthy human subjects. Conclusions We found that MIR155 is upregulated in the endothelium in mouse and men as part of a systemic inflammatory response and might contribute to the pathophysiology of vascular leakage in a Claudin-1-dependent manner. Future studies have to clarify whether MIR155 could be a potential therapeutic target. |
| ArticleNumber | 76 |
| Audience | Academic |
| Author | Thum, Thomas Idowu, Temitayo O. Geffers, Robert Garg, Ankita Etzrodt, Valerie Haller, Hermann van Meurs, Matijs David, Sascha Prasse, Antje Parikh, Samir M. Schenk, Heiko Müller-Deile, Janina Seeliger, Benjamin Stahl, Klaus Pape, Thorben Thamm, Kristina |
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| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/33618730$$D View this record in MEDLINE/PubMed |
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| Cites_doi | 10.1038/sj.jid.5700865 10.1016/j.micinf.2005.12.016 10.1056/NEJMra1208623 10.3390/ijms17010078 10.1093/bioinformatics/btt656 10.1371/journal.pone.0179850 10.1001/jama.2016.0287 10.1161/JAHA.118.009244 10.1097/CCM.0000000000003269 10.1093/toxsci/46.2.300 10.7754/Clin.Lab.2016.160511 10.1186/s40635-018-0203-4 10.1097/CCM.0000000000000524 10.1161/ATVBAHA.111.233189 10.1093/bioinformatics/btp616 10.1155/2019/6714080 10.1097/SHK.0000000000001243 10.1165/rcmb.2011-0289OC 10.1093/bioinformatics/bts635 10.1007/s00441-017-2593-0 10.1186/cc13806 10.3389/fimmu.2018.00057 10.1155/2013/658270 10.1097/CCM.0b013e31825fdc31 10.1016/S0092-8674(04)00045-5 |
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| Keywords | Sepsis Tight junctions Respiratory distress syndrome MicroRNAs Endothelium |
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| References | F Benz (3500_CR20) 2016; 17 H Schenk (3500_CR13) 2017; 369 C Johnston (3500_CR24) 1998; 46 MD Robinson (3500_CR10) 2010; 26 CM Robertson (3500_CR3) 2006; 8 Y Liao (3500_CR9) 2014; 30 S David (3500_CR25) 2012; 40 A Aslan (3500_CR15) 2014; 18 B Zingarelli (3500_CR17) 2019; 51 F Tacke (3500_CR26) 2019; 2019 D Vermette (3500_CR5) 2018; 6 DC Angus (3500_CR2) 2013; 369 A Dobin (3500_CR8) 2013; 29 MH Wong (3500_CR23) 2012; 46 K Thamm (3500_CR12) 2018; 46 DP Bartel (3500_CR6) 2004; 116 JC Pena-Philippides (3500_CR22) 2018; 7 KL Hippen (3500_CR19) 2018; 9 Y Han (3500_CR21) 2016; 62 M Singer (3500_CR1) 2016; 315 T Stiehl (3500_CR11) 2014; 42 3500_CR7 CM Niessen (3500_CR4) 2007; 127 S David (3500_CR14) 2011; 31 N Hanke (3500_CR16) 2013; 2013 D Pfeiffer (3500_CR18) 2017; 12 |
| References_xml | – volume: 127 start-page: 2525 year: 2007 ident: 3500_CR4 publication-title: J Investig Dermatol doi: 10.1038/sj.jid.5700865 – volume: 8 start-page: 1382 year: 2006 ident: 3500_CR3 publication-title: Microbes Infect doi: 10.1016/j.micinf.2005.12.016 – volume: 369 start-page: 840 year: 2013 ident: 3500_CR2 publication-title: N Engl J Med doi: 10.1056/NEJMra1208623 – volume: 17 start-page: 78 year: 2016 ident: 3500_CR20 publication-title: Int J Mol Sci doi: 10.3390/ijms17010078 – volume: 30 start-page: 923 year: 2014 ident: 3500_CR9 publication-title: Bioinformatics (Oxford, England) doi: 10.1093/bioinformatics/btt656 – volume: 12 start-page: e0179850 year: 2017 ident: 3500_CR18 publication-title: PLoS ONE doi: 10.1371/journal.pone.0179850 – volume: 315 start-page: 801 year: 2016 ident: 3500_CR1 publication-title: JAMA doi: 10.1001/jama.2016.0287 – volume: 7 start-page: 13 year: 2018 ident: 3500_CR22 publication-title: J Am Heart Assoc doi: 10.1161/JAHA.118.009244 – volume: 46 start-page: e928 year: 2018 ident: 3500_CR12 publication-title: Crit Care Med doi: 10.1097/CCM.0000000000003269 – volume: 46 start-page: 300 year: 1998 ident: 3500_CR24 publication-title: Toxicol Sci doi: 10.1093/toxsci/46.2.300 – volume: 62 start-page: 2355 year: 2016 ident: 3500_CR21 publication-title: Clin Lab doi: 10.7754/Clin.Lab.2016.160511 – volume: 6 start-page: 37 year: 2018 ident: 3500_CR5 publication-title: Intensive Care Med Exp doi: 10.1186/s40635-018-0203-4 – volume: 42 start-page: e654 year: 2014 ident: 3500_CR11 publication-title: Crit Care Med doi: 10.1097/CCM.0000000000000524 – volume: 31 start-page: 2643 year: 2011 ident: 3500_CR14 publication-title: Arterioscler Thromb Vasc Biol doi: 10.1161/ATVBAHA.111.233189 – volume: 26 start-page: 139 year: 2010 ident: 3500_CR10 publication-title: Bioinformatics (Oxford, England) doi: 10.1093/bioinformatics/btp616 – volume: 2019 start-page: 6714080 year: 2019 ident: 3500_CR26 publication-title: Mediators Inflamm doi: 10.1155/2019/6714080 – volume: 51 start-page: 10 year: 2019 ident: 3500_CR17 publication-title: SHOCK doi: 10.1097/SHK.0000000000001243 – volume: 46 start-page: 641 year: 2012 ident: 3500_CR23 publication-title: Am J Respir Cell Mol Biol doi: 10.1165/rcmb.2011-0289OC – volume: 29 start-page: 15 year: 2013 ident: 3500_CR8 publication-title: Bioinformatics (Oxford, England) doi: 10.1093/bioinformatics/bts635 – volume: 369 start-page: 127 year: 2017 ident: 3500_CR13 publication-title: Cell Tissue Res doi: 10.1007/s00441-017-2593-0 – volume: 18 start-page: 423 year: 2014 ident: 3500_CR15 publication-title: Crit Care (London, England) doi: 10.1186/cc13806 – volume: 9 start-page: 57 year: 2018 ident: 3500_CR19 publication-title: Front Immunol doi: 10.3389/fimmu.2018.00057 – volume: 2013 start-page: 1 year: 2013 ident: 3500_CR16 publication-title: Biomed Res Int doi: 10.1155/2013/658270 – volume: 40 start-page: 3034 year: 2012 ident: 3500_CR25 publication-title: Crit Care Med doi: 10.1097/CCM.0b013e31825fdc31 – volume: 116 start-page: 281 year: 2004 ident: 3500_CR6 publication-title: Cell doi: 10.1016/S0092-8674(04)00045-5 – ident: 3500_CR7 |
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Capillary leakage is a key contributor to the pathological host response to infections. The underlying mechanisms remain incompletely understood,... Capillary leakage is a key contributor to the pathological host response to infections. The underlying mechanisms remain incompletely understood, and the role... Background Capillary leakage is a key contributor to the pathological host response to infections. The underlying mechanisms remain incompletely understood,... Abstract Background Capillary leakage is a key contributor to the pathological host response to infections. The underlying mechanisms remain incompletely... |
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| SubjectTerms | Animal models in research Antibodies Biopsy Critical care Critical Care Medicine Emergency Medicine Endothelium Health aspects Inflammation Intensive Kidneys Laboratory animals Laparotomy Lavage Manufacturers Medical research Medicine Medicine & Public Health MicroRNA MicroRNAs Permeability Properties Proteins Reagents Respiratory distress syndrome Sepsis Tight junctions |
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| Title | Role of endothelial microRNA 155 on capillary leakage in systemic inflammation |
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