ArticleMolecular vision2016
Chondrocyte-derived extracellular matrix suppresses pathogenesis of human pterygium epithelial cells by blocking the NF-κB signaling pathways.
Article in Molecular vision, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
9 citing papers in PubMed, 7 citations in OpenAlex.
- NF-κB signaling in osteoarthritis: integrating mechanical stress, innate immunity, and cartilage degeneration.Frontiers in immunology · 2026Review
- Pterygium-The Good, the Bad, and the Ugly.Cells · 2021Review
- Potential Protective and Therapeutic Roles of the Nrf2 Pathway in Ocular Diseases: An Update.Oxidative medicine and cellular longevity · 2020Review
- Inhibition of osteoclastogenesis by stem cell-derived extracellular matrix through modulation of intracellular reactive oxygen species.Acta biomaterialia · 2018Article
- Local pro-inflammatory cytokine and nitric oxide responses are elevated in patients with pterygium.International journal of immunopathology and pharmacology · 2017Article
- Nrf2, a Potential Therapeutic Target against Oxidative Stress in Corneal Diseases.Oxidative medicine and cellular longevity · 2017Review
- Comparison of fibrin glue and Vicryl sutures in conjunctival autografting for pterygium surgery.Molecular vision · 2017Article
- Exploring the Contribution of Interleukin-12A Genetic Polymorphisms to Pterygium Risk.In vivo (Athens, Greece)Article
- Exploring the Genetic Role of Matrix Metalloproteinase-13 Variants in Pterygium Risk.In vivo (Athens, Greece)Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purposeWe previously have reported that chondrocyte-derived extracellular matrix (CDECM) suppresses the growth of pterygium in athymic nude mice. The aim of this study is to demonstrate the effect of CDECM on the pterygium epithelial cells and molecular signaling pathways in human primary pterygium epithelial cells (hPECs).
methodsHuman conjunctival epithelial cells (hConECs) were used for identification of the effect of CDECM on normal conjunctiva. The effects of CDECM on proliferation were measured with the 3-(4,5-dimethylthiazol-2-yl)-5-(3-carboxy-methoxyphenyl)-2-(4-sulfenyl)-2H-tetrazolium (MTS) assay. Cell migration was evaluated according to the scratch wound closure assay and the Transwell invasion assay. Pterygium-related angiogenesis, inflammation, and extracellular matrix remodeling were analyzed with immunoblot and enzyme-linked immunosorbent assay (ELISA). The level of oxidative stress was detected with 2',7'-dichlorofluorescein diacetate (DCFH-DA). Protein kinase signaling was also analyzed with immunoblot.
resultsCDECM did not show cytotoxicity until 1 mg/ml in the hConECs and hPECs. Cell migration and invasion were markedly reduced by treatment of 1 mg/ml CDECM in the hPECs to 34% of the control, but not in the hConECs. CDECM significantly downregulated matrix metallopeptidase 9 (MMP-9) and fibronectin and upregulated tissue inhibitor of metalloprotease 1 (TIMP-1) and -2 in the hPECs. Angiogenic factors, such as vascular endothelial growth factor (VEGF), antivascular cellular adhesion molecule 1 (VCAM-1), and cluster of differentiation 31 (CD31), and proinflammatory factors, including tumor necrosis factor-α (TNF-α), cyclooxygenase-2 (Cox2), interleukin 6 (IL-6), and prostaglandin E
conclusionsCDECM was markedly effective in pathogenesis of hPECs. CDECM-suppressed migration of hPECs resulted from the inhibition of NF-κB activation and the improvement of Nrf2 induction by blocking the p38 MAPK and PKC signaling pathways.
Indexed as
Identifiers
28050122PMC5204452W2568185177What OpenQuestion holds
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.