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Related Experiment Video

Updated: Jul 11, 2025

Spectral Confocal Imaging of Fluorescently tagged Nicotinic Receptors in Knock-in Mice with Chronic Nicotine Administration
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ERp29 Attenuates Nicotine-Induced Endoplasmic Reticulum Stress and Inhibits Choroidal Neovascularization.

Tu Lu1, Fangfang Xie1, Chuangxin Huang1

  • 1State Key Laboratory of Ophthalmology, Zhongshan Ophthalmic Center, Sun Yat-sen University, Guangdong Provincial Key Laboratory of Ophthalmology and Visual Science, Guangzhou 510060, China.

International Journal of Molecular Sciences
|November 14, 2023
PubMed
Summary

ERp29 protein reduces nicotine-induced endoplasmic reticulum stress and choroidal neovascularization (CNV). This finding offers a potential therapeutic target for age-related macular degeneration (AMD) by mitigating damage in retinal pigment epithelium cells.

Keywords:
ERp29choroidal neovascularizationendoplasmic reticulum stressmacrophage polarizationnicotine

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Area of Science:

  • Ophthalmology
  • Cell Biology
  • Molecular Biology

Background:

  • Nicotine exposure causes endoplasmic reticulum (ER) stress in retinal pigment epithelium (RPE) cells, a key factor in age-related macular degeneration (AMD).
  • ERp29 protein has shown potential in mitigating ER stress and damage in RPE cells.

Purpose of the Study:

  • To investigate the role of ERp29 in nicotine-induced ER stress and choroidal neovascularization (CNV).

Main Methods:

  • Examined ERp29 and GRP78 expression in ARPE-19 cells exposed to nicotine.
  • Investigated the effects of ERp29 overexpression and knockdown on ER stress markers (GRP78, CHOP) and cell viability.
  • Analyzed macrophage polarization in a co-culture system.
  • Assessed the impact of ERp29 on human umbilical vein endothelial cell (HUVEC) function.
  • Evaluated ERp29's effect on CNV in a mouse model.

Main Results:

  • Nicotine exposure increased ERp29 and GRP78 expression in ARPE-19 cells.
  • ERp29 overexpression reduced GRP78 and CHOP levels and modulated macrophage polarization towards M1 markers.
  • ERp29 knockdown decreased cell viability under nicotine stress.
  • Conditioned medium from ERp29-overexpressing cells inhibited HUVEC viability, migration, and tube formation.
  • ERp29 overexpression suppressed nicotine-induced CNV in vivo.

Conclusions:

  • ERp29 plays a protective role against nicotine-induced ER stress and CNV.
  • ERp29 modulates macrophage polarization and inhibits angiogenesis.
  • ERp29 represents a potential therapeutic target for AMD and related conditions.