Open Access

iRHOM2 regulates inflammation and endothelial barrier permeability via CX3CL1

  • Authors:
    • Huiyuan Yan
    • Junsong Wu
    • Huilian Yan
  • View Affiliations

  • Published online on: May 15, 2023     https://doi.org/10.3892/etm.2023.12018
  • Article Number: 319
  • Copyright: © Yan et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

Acute lung injury (ALI) is associated with increased lung inflammation and lung permeability. The present study aimed to determine the role of inactive rhomboid‑like protein 2 (iRHOM2) in ALI in lipopolysaccharide (LPS)‑induced pulmonary microvascular endothelial cell model. Human pulmonary microvascular endothelial cells (HPMVECs) were transfected with small interfering RNA targeting iRHOM2 and C‑X3‑C motif chemokine ligand 1 (CX3CL1) overexpression plasmids and treated with LPS. Cell viability was detected using a Cell Counting Kit‑8 assay, while levels of TNFα, IL‑1β, IL‑6 and p65 were measured by reverse transcription‑quantitative PCR and western blotting. Apoptosis levels were measured using a TUNEL assay. Endothelial barrier permeability was detected, followed by analysis of zonula occludens‑1, vascular endothelial‑cadherin and occludin by immunofluorescence staining or western blotting. The interaction of iRHOM2 and CX3CL1 was analyzed using an immune‑coprecipitation assay. Through bioinformatics analysis, it was found that CX3CL1 was upregulated in the LPS group compared with the control. Kyoto Encyclopedia of Genes and Genomes pathway analysis demonstrated that the TNF signaling pathway affected by iRHOM2 and cytokine‑cytokine receptor interaction, including CX3CL1, served a key role in ALI. HPMVECs treated with LPS exhibited a decrease in cell viability and an increase in inflammation, apoptosis and endothelial barrier permeability, while these effects were reversed by iRHOM2 silencing. However, CX3CL1 overexpression inhibited the effects of iRHOM2 silencing on LPS‑treated HPMVECs. The present study demonstrated a novel role of iRHOM2 as a regulator that affects inflammation, apoptosis and endothelial barrier permeability; this was associated with CX3CL1.
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July-2023
Volume 26 Issue 1

Print ISSN: 1792-0981
Online ISSN:1792-1015

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Spandidos Publications style
Yan H, Wu J and Yan H: iRHOM2 regulates inflammation and endothelial barrier permeability via CX3CL1. Exp Ther Med 26: 319, 2023
APA
Yan, H., Wu, J., & Yan, H. (2023). iRHOM2 regulates inflammation and endothelial barrier permeability via CX3CL1. Experimental and Therapeutic Medicine, 26, 319. https://doi.org/10.3892/etm.2023.12018
MLA
Yan, H., Wu, J., Yan, H."iRHOM2 regulates inflammation and endothelial barrier permeability via CX3CL1". Experimental and Therapeutic Medicine 26.1 (2023): 319.
Chicago
Yan, H., Wu, J., Yan, H."iRHOM2 regulates inflammation and endothelial barrier permeability via CX3CL1". Experimental and Therapeutic Medicine 26, no. 1 (2023): 319. https://doi.org/10.3892/etm.2023.12018