Clinical Microbiology: Open Access

Nitric oxide up-regulates SOD1 mRNA via. Nrf2-independent pathway in a cellular model of amyotrophic lateral sclerosis

Joint Event on 25^th Asia Pacific Biotechnology Congress & 3^rd International Conference on Medical and Clinical Microbiology

May 01-02, 2019 Kyoto, Japan

Omar Gammoh, Pamela Milani, Cristina Cereda and Mauro Ceroni

American University of Madaba, Jordan

Posters & Accepted Abstracts: Clin Microbiol

Abstract:

Introduction & Aim: Amyotrophic Lateral Sclerosis (ALS) is a fatal neurodegenerative disorder that is mainly characterized by a selective loss of motor neurons. Copper, zinc superoxide dismutase, SOD1 is an antioxidant enzyme that is implicated in ALS. Indeed SOD1 gene expression was up regulated in ALS patient tissues. NF-E2 related factor 2 (Nrf2) is a transcriptional factor that is translocate to the nuclear compartment to mediate the regulation of a battery of antioxidant genes by binding to the ARE domain. The aim is to study the effect of NO on SOD1 gene expression and to investigate the role of Nrf2/ARE pathway in SOD1 gene expression after NO treatment in ALS cell line model.

Method: Human neuroblastoma SH-SY5Y cells were treated with NO (100 uM, 200 uM and 500 uM) or 8Br-cGMP for 18 hours. SOD1 gene expression was measured via. real-time PCR. Nrf2 shuttling and binding were assessed through western blot and electro-mobility shift assay respectively.

Result: Nitric oxide up-regulated SOD1 gene expression in a concentration dependent manner. However the Nrf2/ARE pathway was not activated.

Conclusion: This study fills a gap in the literature by demonstrating that an increase in NO levels is directly associated to an increase in SOD1 gene.

Biography :

E-mail: o.gammouh@aum.edu.jo