ArticleAmerican journal of respiratory cell and molecular biology2012
Regulation of Rela/p65 and endothelial cell inflammation by proline-rich tyrosine kinase 2.
Article in American journal of respiratory cell and molecular biology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 29 citations in OpenAlex.
- Pharmacological Blockade of Hypoxia-Driven Autophagy: A Therapeutic Strategy to Limit Endothelial Activation and Thrombosis.ACS pharmacology & translational science · 2026Article
- Tuberous sclerosis complex 2 association with RelA/p65 is critical for NF-κB activation and endothelial cell inflammation.Cell communication and signaling : CCS · 2026Article
- Differential plasma proteome analysis reveals key proteins associated with insulin resistance in acne vulgaris patients.Scientific reports · 2025Article
- Single cell transcriptomics in a treatment-segregated cohort exposes a STAT3-regulated therapeutic gap in idiopathic pulmonary fibrosis.bioRxiv : the preprint server for biology · 2025Article
- PTPN20 promotes metastasis through activating NF-κB signaling in triple-negative breast cancer.Breast cancer research : BCR · 2024Article
- Transport of Non-Steroidal Anti-Inflammatory Drugs across an Oral Mucosa Epithelium In Vitro Model.Pharmaceutics · 2024Article
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- Genetics of macrovascular complications in type 2 diabetes.World journal of diabetes · 2021Review
- The Inflammatory Profile of CTEPH-Derived Endothelial Cells Is a Possible Driver of Disease Progression.Cells · 2021Article
- Redox Regulation, Oxidative Stress, and Inflammation in Group 3 Pulmonary Hypertension.Advances in experimental medicine and biology · 2021Review
- Autophagy protein ATG7 is a critical regulator of endothelial cell inflammation and permeability.Scientific reports · 2020Article
- Critical role of autophagy regulator Beclin1 in endothelial cell inflammation and barrier disruption.Cellular signalling · 2019Article
- Importins α and β signaling mediates endothelial cell inflammation and barrier disruption.Cellular signalling · 2018Article
- Pyk2 phosphorylation of VE-PTP downstream of STIM1-induced CaAmerican journal of physiology. Lung cellular and molecular physiology · 2017Article
- Phospholipase C-ε signaling mediates endothelial cell inflammation and barrier disruption in acute lung injury.American journal of physiology. Lung cellular and molecular physiology · 2016Article
- Proline-rich tyrosine kinase 2 downregulates peroxisome proliferator-activated receptor gamma to promote hypoxia-induced pulmonary artery smooth muscle cell proliferation.Pulmonary circulation · 2016Article
- Autophagy-induced RelB/p52 activation mediates tumour-associated macrophage repolarisation and suppression of hepatocellular carcinoma by natural compound baicalin.Cell death & disease · 2015Article
- Regulation of endothelial cell inflammation and lung polymorphonuclear lymphocyte infiltration by transglutaminase 2.Shock (Augusta, Ga.) · 2014Article
- HIV-1 Tat C phosphorylates VE-cadherin complex and increases human brain microvascular endothelial cell permeability.BMC neuroscience · 2014Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
We investigated the role of proline-rich tyrosine kinase 2 (Pyk2) in the mechanism of NF-κB activation and endothelial cell (EC) inflammation induced by thrombin, a procoagulant serine protease released in high amounts during sepsis and other inflammatory conditions. Stimulation of ECs with thrombin resulted in a time-dependent activation of Pyk2. RNA interference knockdown of Pyk2 attenuated thrombin-induced activity of NF-κB and expression of its target genes, vascular cell adhesion molecule-1 and monocyte chemoattractant protein-1. Pyk2 knockdown impaired thrombin-induced activation of IκB kinase (IKK) and phosphorylation (Ser32 and Ser36) of IkappaBα, but, surprisingly, failed to prevent IκBα degradation. However, depletion of IKKα or IKKβ was effective in inhibiting IκBα phosphorylation/degradation, as expected. Intriguingly, Pyk2 knockdown impaired nuclear translocation and DNA binding of RelA/p65, despite the inability to prevent IκBα degradation. In addition, Pyk2 knockdown was associated with inhibition of RelA/p65 phosphorylation at Ser536, which is important for transcriptional activity of RelA/p65. Depletion of IKKα or IKKβ each impaired RelA/p65 phosphorylation. Taken together, these data identify Pyk2 as a critical regulator of EC inflammation by virtue of engaging IKK to promote the release and the transcriptional capacity of RelA/p65, and, additionally, by its ability to facilitate the nuclear translocation of the released RelA/p65. Thus, specific targeting of Pyk2 may be an effective anti-inflammatory strategy in vascular diseases associated with EC inflammation and intravascular coagulation.
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Registered trials
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