YM155 inhibits retinal pigment epithelium cell survival through EGFR/MAPK signaling pathway
Author:
Corresponding Author:

Xiao-Dong Chen. Department of Ophthalmology, Xi'an No.1 Hospital, Xi'an 710002, Shaanxi Province, China. cxd390203850@163.com

Affiliation:

Clc Number:

Fund Project:

Supported by the Natural Science Foundation of Shaanxi Province, China (No.2018JM7040); the Science and Technology Planned Projects of Xi'an City, China [No.20YXXJ008(4)]; the Health Research Personnel Training Project of Xi'an Health Commission, China (No.J201901009).

  • Article
  • |
  • Figures
  • |
  • Metrics
  • |
  • Reference
  • |
  • Related
  • |
  • Cited by
  • |
  • Materials
  • |
  • Comments
    Abstract:

    AIM: To investigate YM155's effect on retinal pigment epithelium (RPE) cells' viability and the potential regulatory mechanisms. METHODS: Human immortalized RPE cell lines (ARPE-19 cell line) were processed with YM155 and epidermal growth factor (EGF). ARPE-19 cell viability was detected by methyl thiazolyl tetrazolium assay, and apoptosis was tested by flow cytometry assay. ARPE-19 cell proliferation was assessed with bromodeoxyuridine tagged incorporation assay, and migration ability was evaluated via a wound-healing assay. Epidermal growth factor receptor (EGFR)/MAPK pathway proteins were tested via immunoblotting. EGFR localization was examined by immunofluorescence assay. RESULTS: YM155 suppressed ARPE-19 cells' viability in a time and concentration-dependent manner. A high dose of YM155 caused a small amount of ARPE-19 cell death. YM155 significantly diminished the ARPE-19 cells' proliferative and migrative capacity. YM155 down-regulated total EGFR and phosphorylated external signal-regulated protein kinase (ERK), and it up-regulated the phosphorylation of P38MAPK and c-Jun N-terminal kinase (JNK). YM155 induced endocytosis of EGFR in ARPE-19 cell. YM155 also attenuated EGF-induced ARPE-19 cells' proliferative and migrative capacity. Moreover, YM155 significantly decreased the expression of phosphorylated EGFR and ERK after treated by EGF. CONCLUSION: YM155 inhibits RPE cell survival, the cell proliferative and migrative capacity, and it effectuates a small amount of cell death through the EGFR/MAPK signaling pathway. YM155 might, therefore, be an agent to prevent and treat abnormal RPE cell survival in proliferative vitreoretinopathy.

    Reference
    Related
    Cited by
Get Citation

Teng Li, Hong-Bing Zhang, Jia-Min Meng, et al. YM155 inhibits retinal pigment epithelium cell survival through EGFR/MAPK signaling pathway. Int J Ophthalmol, 2021,14(4):489-496

Copy
Share
Article Metrics
  • Abstract:
  • PDF:
  • HTML:
  • Cited by:
Publication History
  • Received:December 07,2020
  • Revised:January 14,2021
  • Adopted:
  • Online: February 25,2021
  • Published: