GAS5 Gene Expression and IL-6 in Rheumatoid Arthritis

Overview

This study aims to investigate the expression of Growth Arrest-Specific 5 (GAS5) , a long non-coding RNA , in patients with Rheumatoid Arthritis compared with healthy individuals. The study will also assess the level of Interlukin-6 (IL-6) in the blood and explore the relationship between GAS5 expression and IL-6 levels in Rheumatoid Arthritis

Rheumatoid arthritis (RA) is a chronic systemic autoimmune disease characterized by persistent inflammation of the joints and may result in progressive joint damage and functional impairment. The mechanisms underlying the development and progression of RA involve complex interactions between immune, inflammatory, and molecular pathways. Long non-coding RNAs (lncRNAs) are regulatory RNA molecules that can influence gene expression and participate in various biological processes, including immune regulation and inflammation. Growth Arrest-Specific 5 (GAS5) is a long non-coding RNA that has been implicated in the regulation of inflammatory and immune-related processes and may have a role in autoimmune diseases. Interleukin-6 (IL-6) is an important pro-inflammatory cytokine involved in the inflammatory response and pathogenesis of rheumatoid arthritis. Assessment of IL-6 levels may provide information regarding the inflammatory status of patients with RA. This observational study will compare GAS5 expression and blood IL-6 levels between patients with rheumatoid arthritis and healthy controls. Blood samples will be collected from eligible participants. GAS5 expression will be assessed using quantitative real-time polymerase chain reaction (qRT-PCR), while IL-6 levels will be measured using an enzyme-linked immunosorbent assay (ELISA). The study will also examine the relationship between these molecular and inflammatory markers and selected clinical and laboratory characteristics of rheumatoid arthritis. The findings may contribute to a better understanding of the molecular mechanisms involved in RA and the potential role of GAS5 and IL-6 in the disease.

Conditions

Eligibility

Outcomes

Central Contacts