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The complement C3a‑C3aR and C5a‑C5aR pathways promote viability and inflammation of human retinal pigment epithelium cells by targeting NF‑κB signaling

  • Authors:
    • Shasha Luo
    • Huiyan Xu
    • Xuechun Gong
    • Jinyan Shen
    • Xuan Chen
    • Zhifeng Wu

  • View Affiliations

  • Published online on: June 7, 2022     https://doi.org/10.3892/etm.2022.11420
  • Article Number: 493

  • Copyright: © Luo et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

Retinal detachment (RD) and its special form of rhegmatogenous RD associated with choroidal detachment (RRDCD) feature similar pathological alterations, including enhanced retinal cell inflammation. Although the importance of the complement components C3a and C5a and their corresponding receptors in retinal maintenance has been demonstrated, the relevance of these molecules to the pathogenesis of RD or RRDCD remains to be investigated. The contents of C3a, C5a and inflammatory factors, such as TNF‑α, IL‑1β, IL‑6 and prostaglandin (PG)E2, in related clinical samples were examined by ELISA. Subsequently, human retinal pigment epithelial (HRPE) cells were subjected to challenge with the C3a and C5a recombinant proteins with or without C3a and C5a antagonists and NF‑κB inhibitor, and the cell viability and inflammatory cytokines were then determined by a Cell Counting Kit‑8 assay and ELISA, respectively. In addition, reverse transcription‑quantitative PCR and western blot analyses were utilized to examine the mRNA or/and protein levels of C3a and its receptor C3aR, as well as C5a and its receptor C5aR, and NF‑κB. In addition, the correlation of C3a and C5a with the aforementioned inflammatory factors was analyzed. The inflammatory factor levels of C3a and C5a were considerably elevated in patients with RRDCD compared to those in the controls. Consistently, C3a and C5a treatment led to increased cell viability and aggravated inflammation in HRPE cells. Accordingly, C3a and C5a induced upregulation of their corresponding receptors C3aR and C5aR, which was in turn observed to be linked to the activation of the NF‑κB signaling pathway. Furthermore, there was a positive correlation of the complements C3a and C5a with individual TNF‑α, IL‑1β, IL‑6 and PGE2. Taken together, the C3a‑C3aR and C5a‑C5aR pathways were indicated to promote cell viability and inflammation of HRPE cells by targeting the NF‑κB signaling pathway.
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August-2022
Volume 24 Issue 2

Print ISSN: 1792-0981
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Spandidos Publications style
Luo S, Xu H, Gong X, Shen J, Chen X and Wu Z: The complement C3a‑C3aR and C5a‑C5aR pathways promote viability and inflammation of human retinal pigment epithelium cells by targeting NF‑κB signaling. Exp Ther Med 24: 493, 2022
APA
Luo, S., Xu, H., Gong, X., Shen, J., Chen, X., & Wu, Z. (2022). The complement C3a‑C3aR and C5a‑C5aR pathways promote viability and inflammation of human retinal pigment epithelium cells by targeting NF‑κB signaling. Experimental and Therapeutic Medicine, 24, 493. https://doi.org/10.3892/etm.2022.11420
MLA
Luo, S., Xu, H., Gong, X., Shen, J., Chen, X., Wu, Z."The complement C3a‑C3aR and C5a‑C5aR pathways promote viability and inflammation of human retinal pigment epithelium cells by targeting NF‑κB signaling". Experimental and Therapeutic Medicine 24.2 (2022): 493.
Chicago
Luo, S., Xu, H., Gong, X., Shen, J., Chen, X., Wu, Z."The complement C3a‑C3aR and C5a‑C5aR pathways promote viability and inflammation of human retinal pigment epithelium cells by targeting NF‑κB signaling". Experimental and Therapeutic Medicine 24, no. 2 (2022): 493. https://doi.org/10.3892/etm.2022.11420