ArticlePloS one2012
Biological effects of cigarette smoke in cultured human retinal pigment epithelial cells.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
21 citing papers in PubMed, 28 citations in OpenAlex.
- A critical role for mitochondrial dynamics in cigarette smoke condensate-induced RPE senescence.Free radical biology & medicine · 2026Article
- H105A peptide eye drops promote photoreceptor survival in murine and human models of retinal degeneration.Communications medicine · 2025Article
- Cigarette smoke extract induces ferroptosis in human retinal pigment epithelial cells.Heliyon · 2024Article
- H105A peptide eye drops promote photoreceptor survival in murine and human models of retinal degeneration.bioRxiv : the preprint server for biology · 2024Article
- Aqueous humor perturbations in chronic smokers: a proteomic study.Scientific reports · 2024Article
- ERp29 Attenuates Nicotine-Induced Endoplasmic Reticulum Stress and Inhibits Choroidal Neovascularization.International journal of molecular sciences · 2023Article
- Fabrication and Evaluation of Gellan Gum/Hyaluronic Acid Hydrogel for Retinal Tissue Engineering Biomaterial and the Influence of Substrate Stress Relaxation on Retinal Pigment Epithelial Cells.Molecules (Basel, Switzerland) · 2022Article
- A Pilot Application of an iTRAQ-Based Proteomics Screen Estimates the Effects of Cigarette Smokers' Serum on RPE Cells With AMD High-Risk Alleles.Translational vision science & technology · 2022Article
- Article
- Oxidative stress affects retinal pigment epithelial cell survival through epidermal growth factor receptor/AKT signaling pathway.International journal of ophthalmology · 2017Article
- Cigarette smoke induced autophagy-impairment regulates AMD pathogenesis mechanisms in ARPE-19 cells.PloS one · 2017Article
- Strand and Cell Type-specific Function of microRNA-126 in Angiogenesis.Molecular therapy : the journal of the American Society of Gene Therapy · 2016Article
- Oxidative stress-induced premature senescence dysregulates VEGF and CFH expression in retinal pigment epithelial cells: Implications for Age-related Macular Degeneration.Redox biology · 2016Article
- Airway Exposure to E-Cigarette Vapors Impairs Autophagy and Induces Aggresome Formation.Antioxidants & redox signaling · 2016Article
- 4-Acetoxyphenol Prevents RPE Oxidative Stress-Induced Necrosis by Functioning as an NRF2 Stabilizer.Investigative ophthalmology & visual science · 2015Article
- Tapping Stem Cells to Target AMD: Challenges and Prospects.Journal of clinical medicine · 2015Review
- Article
- Smoke exposure causes endoplasmic reticulum stress and lipid accumulation in retinal pigment epithelium through oxidative stress and complement activation.The Journal of biological chemistry · 2014Article
- Role of unfolded protein response dysregulation in oxidative injury of retinal pigment epithelial cells.Antioxidants & redox signaling · 2014Article
- 2-ethylpyridine, a cigarette smoke component, causes mitochondrial damage in human retinal pigment epithelial cells in vitro.Indian journal of ophthalmology · 2014Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The goal of the present study was to determine whether treatment with cigarette smoke extract (CSE) induces cell loss, cellular senescence, and extracellular matrix (ECM) synthesis in primary human retinal pigment epithelial (RPE) cells. Primary cultured human RPE cells were exposed to 2, 4, 8, and 12% of CSE concentration for 24 hours. Cell loss was detected by cell viability assay. Lipid peroxidation was assessed by loss of cis-parinaric acid (PNA) fluorescence. Senescence-associated ß-galactosidase (SA-ß-Gal) activity was detected by histochemical staining. Expression of apolipoprotein J (Apo J), connective tissue growth factor (CTGF), fibronectin, and laminin were examined by real-time PCR, western blot, or ELISA experiments. The results showed that exposure of cells to 12% of CSE concentration induced cell death, while treatment of cells with 2, 4, and 8% CSE increased lipid peroxidation. Exposure to 8% of CSE markedly increased the number of SA-ß-Gal positive cells to up to 82%, and the mRNA expression of Apo J, CTGF, and fibronectin by approximately 3-4 fold. Treatment with 8% of CSE also increased the protein expression of Apo J and CTGF and the secretion of fibronectin and laminin. Thus, treatment with CSE can induce cell loss, senescent changes, and ECM synthesis in primary human RPE cells. It may be speculated that cigarette smoke could be involved in cellular events in RPE cells as seen in age-related macular degeneration.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.