The nuclear-factor kappaB pathway is activated in pterygium

Area of Science:

• Ophthalmology
• Molecular Biology
• Immunology

Background:

• Pterygium is a common ocular surface disease with an unclear pathogenesis.
• Nuclear factor kappa B (NF-κB) is a key transcription factor involved in immune responses and inflammation.

Purpose of the Study:

• To investigate the role of NF-κB transcription factors in the pathogenesis of pterygium.
• To determine if NF-κB is activated in pterygium tissues and how it is regulated by inflammatory stimuli.

Main Methods:

• Comparative analysis of surgically excised pterygia and normal conjunctiva tissues.
• Evaluation of NF-κB activation using Western blot, ELISA, and DNA-binding assays.
• In vitro studies on pterygium fibroblasts treated with TNF-α, assessing NF-κB pathway activation and target gene expression via immunocytochemistry, Western blot, ELISA, and real-time PCR.

Main Results:

• Increased IκBα phosphorylation and decreased IκBα expression in pterygia tissues, indicating NF-κB activation.
• Enhanced nuclear translocation and DNA-binding capacity of NF-κB subunits (RelA, p50) in pterygium fibroblasts upon TNF-α stimulation.
• Upregulation of NF-κB target genes, including those involved in inflammation (RANTES, MCP-1, ENA-78) and matrix degradation (MMP-1, MMP-2, MMP-3), was more pronounced in pterygium fibroblasts compared to tenon fibroblasts.

Conclusions:

• The NF-κB pathway is demonstrably activated in pterygium tissues, suggesting its involvement in the disease's pathogenesis.
• Both canonical and noncanonical NF-κB pathways can be activated by TNF-α in pterygium fibroblasts.
• This activation leads to the upregulation of specific target genes, potentially contributing to pterygium development and progression.