Targeting synergetic endothelial inflammation by inhibiting NFKB and JAK-STAT pathways

Summary: Multiple systemic vascular inflammatory disorders are associated with endothelial dysfunction and elevated levels of TNFα and IFNγ. Combined TNFα and IFNγ stimulation induces synergetic hyperinflammation in endothelial cells (ECs) through the activation of the NFKB and JAK/STAT pathways. He...

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Main Authors: Stijn A. Groten, Pieter Langerhorst, Georgios Malamas, Alastair Barraclough, Arie J. Hoogendijk, Maartje van den Biggelaar
Format: Article
Language:English
Published: Elsevier 2025-09-01
Series:iScience
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Online Access:http://www.sciencedirect.com/science/article/pii/S2589004225015688
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author Stijn A. Groten
Pieter Langerhorst
Georgios Malamas
Alastair Barraclough
Arie J. Hoogendijk
Maartje van den Biggelaar
author_facet Stijn A. Groten
Pieter Langerhorst
Georgios Malamas
Alastair Barraclough
Arie J. Hoogendijk
Maartje van den Biggelaar
author_sort Stijn A. Groten
collection DOAJ
description Summary: Multiple systemic vascular inflammatory disorders are associated with endothelial dysfunction and elevated levels of TNFα and IFNγ. Combined TNFα and IFNγ stimulation induces synergetic hyperinflammation in endothelial cells (ECs) through the activation of the NFKB and JAK/STAT pathways. Here, we assess how targeting these pathways affects EC inflammation. Using mass spectrometry based proteomics, we investigate system-wide effects of TNFα- and IFNγ-stimulated Endothelial Colony Forming Cells (ECFCs) in combination with inhibitors targeting NFKB and JAK/STAT pathways. JAK1 inhibitor itacitinib blocked IFNγ-, but not TNFα-induced proteomic responses. IKK2/STAT3 inhibitor TPCA1 attenuated both responses. Most TNFα+IFNγ-induced proteins, such as pyroptosis mediators, chemokines, and Weibel-Palade Body content, were inhibited by both inhibitors, highlighting their synergetic dependency on both pathways. Imaging of Von Willebrand Factor (VWF) revealed an extracellular VWF network induced by combined stimulation, a phenotype which was reverted by both inhibitors. This study provides a preliminary basis for inhibiting endothelial inflammation in vascular inflammatory disorders.
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spelling doaj-art-044d04776d5847e5a011e3c2dba9d8d32025-08-20T05:07:27ZengElsevieriScience2589-00422025-09-0128911330710.1016/j.isci.2025.113307Targeting synergetic endothelial inflammation by inhibiting NFKB and JAK-STAT pathwaysStijn A. Groten0Pieter Langerhorst1Georgios Malamas2Alastair Barraclough3Arie J. Hoogendijk4Maartje van den Biggelaar5Department of Molecular Hematology, Sanquin Research, Plesmanlaan 125, 1066 CX Amsterdam, the NetherlandsDepartment of Molecular Hematology, Sanquin Research, Plesmanlaan 125, 1066 CX Amsterdam, the NetherlandsDepartment of Molecular Hematology, Sanquin Research, Plesmanlaan 125, 1066 CX Amsterdam, the NetherlandsDepartment of Molecular Hematology, Sanquin Research, Plesmanlaan 125, 1066 CX Amsterdam, the NetherlandsDepartment of Molecular Hematology, Sanquin Research, Plesmanlaan 125, 1066 CX Amsterdam, the NetherlandsDepartment of Molecular Hematology, Sanquin Research, Plesmanlaan 125, 1066 CX Amsterdam, the Netherlands; Corresponding authorSummary: Multiple systemic vascular inflammatory disorders are associated with endothelial dysfunction and elevated levels of TNFα and IFNγ. Combined TNFα and IFNγ stimulation induces synergetic hyperinflammation in endothelial cells (ECs) through the activation of the NFKB and JAK/STAT pathways. Here, we assess how targeting these pathways affects EC inflammation. Using mass spectrometry based proteomics, we investigate system-wide effects of TNFα- and IFNγ-stimulated Endothelial Colony Forming Cells (ECFCs) in combination with inhibitors targeting NFKB and JAK/STAT pathways. JAK1 inhibitor itacitinib blocked IFNγ-, but not TNFα-induced proteomic responses. IKK2/STAT3 inhibitor TPCA1 attenuated both responses. Most TNFα+IFNγ-induced proteins, such as pyroptosis mediators, chemokines, and Weibel-Palade Body content, were inhibited by both inhibitors, highlighting their synergetic dependency on both pathways. Imaging of Von Willebrand Factor (VWF) revealed an extracellular VWF network induced by combined stimulation, a phenotype which was reverted by both inhibitors. This study provides a preliminary basis for inhibiting endothelial inflammation in vascular inflammatory disorders.http://www.sciencedirect.com/science/article/pii/S2589004225015688BiochemistryCell biologyProteomics
spellingShingle Stijn A. Groten
Pieter Langerhorst
Georgios Malamas
Alastair Barraclough
Arie J. Hoogendijk
Maartje van den Biggelaar
Targeting synergetic endothelial inflammation by inhibiting NFKB and JAK-STAT pathways
iScience
Biochemistry
Cell biology
Proteomics
title Targeting synergetic endothelial inflammation by inhibiting NFKB and JAK-STAT pathways
title_full Targeting synergetic endothelial inflammation by inhibiting NFKB and JAK-STAT pathways
title_fullStr Targeting synergetic endothelial inflammation by inhibiting NFKB and JAK-STAT pathways
title_full_unstemmed Targeting synergetic endothelial inflammation by inhibiting NFKB and JAK-STAT pathways
title_short Targeting synergetic endothelial inflammation by inhibiting NFKB and JAK-STAT pathways
title_sort targeting synergetic endothelial inflammation by inhibiting nfkb and jak stat pathways
topic Biochemistry
Cell biology
Proteomics
url http://www.sciencedirect.com/science/article/pii/S2589004225015688
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