ArticlePathobiology : journal of immunopathology, molecular and cellular biology2010
Fractalkine-induced endothelial cell migration requires MAP kinase signaling.
Article in Pathobiology : journal of immunopathology, molecular and cellular biology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 33 citations in OpenAlex.
- Review
- Fractalkine (Chemokine CX3CL1) Signaling During Placentation and Placental Function.International journal of molecular sciences · 2026Review
- MAPK/ERK signaling pathway in rheumatoid arthritis: mechanisms and therapeutic potential.PeerJ · 2025Review
- Chemokine CX3CL1 (Fractalkine) Signaling and Diabetic Encephalopathy.International journal of molecular sciences · 2024Review
- CX3CL1 (Fractalkine)-CX3CR1 Axis in Inflammation-Induced Angiogenesis and Tumorigenesis.International journal of molecular sciences · 2024Review
- Contactomics of Microglia and Intercellular Communication.Advances in neurobiology · 2024Review
- CX3CL1 Worsens Cardiorenal Dysfunction and Serves as a Therapeutic Target of Canagliflozin for Cardiorenal Syndrome.Frontiers in pharmacology · 2022Article
- Chemokines orchestrate tumor cells and the microenvironment to achieve metastatic heterogeneity.Cancer metastasis reviews · 2021Review
- Inflammatory Mediators and Pain in Endometriosis: A Systematic Review.Biomedicines · 2021Review
- Article
- Fractalkine/CX3CL1 in Neoplastic Processes.International journal of molecular sciences · 2020Review
- Aspirin modulates the inflammatory response in a thrombus‑stimulated LMVEC model.International journal of molecular medicine · 2018Article
- Aspirin Inhibits LPS-Induced Expression of PI3K/Akt, ERK, NF-κB, CX3CL1, and MMPs in Human Bronchial Epithelial Cells.Inflammation · 2016Article
- IL-17A Contributes to the Pathogenesis of Endometriosis by Triggering Proinflammatory Cytokines and Angiogenic Growth Factors.Journal of immunology (Baltimore, Md. : 1950) · 2015Article
- Fractalkine neutralization improves cardiac function after myocardial infarction.Experimental physiology · 2015Article
- The chemokine CX3CL1 (fractalkine) and its receptor CX3CR1: occurrence and potential role in osteoarthritis.Archivum immunologiae et therapiae experimentalis · 2014Review
- Article
- Endothelin-1 activation of the endothelin B receptor modulates pulmonary endothelial CX3CL1 and contributes to pulmonary angiogenesis in experimental hepatopulmonary syndrome.The American journal of pathology · 2014Article
- Mitogen-activated protein kinase phosphatase-1 promotes neovascularization and angiogenic gene expression.Arteriosclerosis, thrombosis, and vascular biology · 2014Article
- Elevated fractalkine in patients with obstructive sleep apnea hypopnea syndrome.Sleep & breathing = Schlaf & Atmung · 2013Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
BACKGROUND/
aimsAngiogenesis is a well-established characteristic in the rheumatoid arthritis (RA) synovial pannus. We have previously demonstrated that fractalkine (Fkn/ CX3CL1) expression is significantly increased in the RA joint and that fractalkine induces angiogenesis. In this work we studied mechanisms through which Fkn functions as an angiogenic mediator.
methodsHuman microvascular endothelial cells (HMVECs) and human umbilical vein endothelial cells (HUVECs) were stimulated with Fkn and analyzed by Western blotting or stained with Alexa Fluor 488 phalloidin for F-actin to characterize the time frame of cytoskeletal rearrangement. Fkn-induced HUVEC chemotaxis was performed in the presence and absence of MAP kinase inhibitors.
resultsPhalloidin staining of F-actin revealed significant cytoskeletal rearrangements in HUVECs and HMVECs starting as early as 10 min after Fkn stimulation. Western blotting demonstrated that HUVEC and HMVEC stimulation with Fkn for 1-30 min resulted in phosphorylation of JNK. Fkn also induces significant phosphorylation of Erk 1/2 in HUVECs over a time course ranging from 1 to 15 min. A somewhat similar time course (5-15 min) was detected for Erk 1/2 phosphorylation in HMVECs. Inhibitors of either JNK or Erk 1/2 nearly abolish Fkn-induced HUVEC migration.
conclusionsWe demonstrate that Fkn induces significant alterations in cytoskeletal structure and specifically activates the MAP kinases, JNK and Erk 1/2, both of which appear necessary for endothelial cell migration. Our results suggest that the endogenous Fkn present in the RA joint may induce angiogenesis through activation of the JNK and Erk 1/2 pathways.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.