Volume 12, Issue 4 (Vol.12 No.4 Jan 2024)                   rbmb.net 2024, 12(4): 512-521 | Back to browse issues page


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Abusree Ahmed A, Fayez Hasa S, Ahmed Rashed L, Ragab Abd ELAzem N, Shehata Mohamed R, Mostafa Gharib Mohamed D. The Potential Association Between microRNA 135-5P and p62 and Their Effect on NRF2 Pathway in Multiple Sclerosis. rbmb.net 2024; 12 (4) :512-521
URL: http://rbmb.net/article-1-1188-en.html
Medical Biochemistry and Molecular Biology Department, Unit of Biochemistry and Molecular Biology, Faculty of Medicine, Cairo University, Cairo, Egypt.
Abstract:   (1478 Views)
Background: Multiple Sclerosis (MS) is a prevalent non-traumatic disabling disease affecting young adults, characterized by complexity in its pathogenesis. Nuclear factor erythroid 2-Related Factor 2 (NRF2) serves as a crucial transcriptional regulator of anti-inflammatory and antioxidant enzymes, influenced by the ubiquitous protein p62. It acts as a scaffold directing substrates to autophagosomes. This study aims to explore the potential association between microRNA 135-5p and p62 and their impact on inflammation and oxidative stress through the NRF2 pathway in MS.

Methods: The study included 30 healthy controls and 60 MS patients (relapsing-remitting and secondary progressive). Real-time PCR was employed for the detection of Nrf2, p62, miRNA135-5P, and NF-κB in serum, while p53 levels were determined using ELISA.

Results: Nrf2 and p62 expression was significantly downregulated in the MS group compared to controls. Conversely, miRNA135-5P, NF-κB expression, and P53 levels were significantly elevated in the MS group.

Conclusion: This study reveals a potential association between miRNA 135-5p and p62, indicating their role in the pathogenesis of MS. Results suggest that miRNA 135-5p and p62 may influence inflammation and oxidative stress in MS through the NRF2 pathway, potentially mediated by NF-κB and p53.

Full-Text [PDF 345 kb]   (424 Downloads)    
Type of Article: Original Article | Subject: Molecular Biology
Received: 2023/06/6 | Accepted: 2023/09/30 | Published: 2024/07/2

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