ArticleKidney research and clinical practice2017
A calpain inhibitor protects against fractalkine production in lipopolysaccharide-treated endothelial cells.
Article in Kidney research and clinical practice, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 9 citations in OpenAlex.
- Article
- Escherichia coli HPI-induced duodenitis through ubiquitin regulation of the TLR4/NF-κB pathway.BMC veterinary research · 2025Article
- 3D-Printed Polymeric Biomaterials for Health Applications.Advanced healthcare materials · 2025Review
- Body Surface Potential Mapping: A Perspective on High-Density Cutaneous Electrophysiology.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Review
- Alpha-1 antitrypsin inhibits fractalkine-mediated monocyte-lung endothelial cell interactions.American journal of physiology. Lung cellular and molecular physiology · 2023Article
- Caspases help to spread the message via extracellular vesicles.The FEBS journal · 2023Review
- DNA Hypermethylation-Regulated CX3CL1 Reducing T Cell Infiltration Indicates Poor Prognosis in Wilms Tumour.Frontiers in oncology · 2022Article
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundFractalkine (CX3CL1) is a chemokine with a unique CX3C motif and is produced by endothelial cells stimulated with lipopolysaccharide (LPS), tumor necrosis factor (TNF)-α, interleukin (IL)-1, and interferon-γ. There have been several reports that the caspase/calpain system is activated in endotoxemia, which leads to cellular apoptosis and acute inflammatory processes. We aimed to determine the role of the caspase/calpain system in cell viability and regulation of fractalkine production in LPS-treated endothelial cells.
methodsHuman umbilical vein endothelial cells (HUVECs) were stimulated with 0.01-100 μg/mL of LPS to determine cell viability. The changes of CX3CL1 expression were compared in control, LPS (1 μg/mL)-, IL-1α (1 μg/mL)-, and IL-1β (1 μg/mL)-treated HUVECs. Cell viability and CX3CL1 production were compared with 50 μM of inhibitors of caspase-1, caspase-3, caspase-9, and calpain in LPS-treated HUVECs.
resultsCell viability was significantly decreased from 1 to 100 μg/mL of LPS. Cell viability was significantly restored with inhibitors of caspase-1, caspase-3, caspase-9, and calpain in LPS-treated HUVECs. The expression of CX3CL1 was highest in IL-1β-treated HUVECs. CX3CL1 production was highly inhibited with a calpain inhibitor and significantly decreased with the individual inhibitors of caspase-1, caspase-3, and caspase-9.
conclusionThe caspase/calpain system is an important modulator of cell viability and CX3CL1 production in LPS-treated endothelial cells.
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