Exploration of the Role of Mitochondria in Stroke

Mitochondria have both a pro-neuronal growth and pro-neuronal death role during a stroke. On the one hand, mitochondria generate ATP to maintain normal neuronal function, on the other hand, mitochondria generate reactive oxygen species (ROS), causing oxidative stress-induced neuronal damage. Although mitochondria have been relatively well studied during a stroke attack, lots of mysteries remain unsolved. Ace Therapeutics provides a full service to explore the mechanisms of mitochondrial action during the stroke attack from the perspectives of oxidative stress, mitophagy, and mitochondria-dependent apoptosis.

Exploration of the Role of Oxidative Stress in Stroke

Mitochondria are the main source of ROS production. Given that after an ischemic stroke attack, mitochondria produce large amounts of ROS, and ROS can destroy lipids, proteins, and nucleic acids in cells and also trigger multiple molecular signaling pathways to further worsen stroke, Ace Therapeutics established in vitro and in vivo stroke models and related assay services to investigate the effects of ROS on the pathological process of stroke, including but not limited to

• Glutathione assays
• Glutathione reductase assays
• Glutathione S-transferase assays
• Total antioxidant capacity assays
• Peroxidase activity assays
• Hydroxyl free radical scavenging capacity assays

Exploration of the Role of Mitophagy in Stroke

The role of mitophagy in stroke has not been well disclosed. For this reason, Ace Therapeutics offers a comprehensive exploration service to disclose the role of mitophagy in stroke.

• To explore the role of NIX, BNIP3, and other proteins in autophagy, we establish suitable in vitro and in vivo stroke models and also offer various assays for the corresponding proteins.
• The role of ROS in the regulation of autophagy, especially in PINK1-Parkin-dependent mitophagy, is unclear. In this regard, we have successfully established gene knockdown or overexpression technologies, along with the service of custom antibodies, to deeply explore the function of ROS on mitophagy regulation.
• Since mitochondrial permeability transition is one of the fundamental events of mitophagy, and the occurrence of stroke alters mitochondrial permeability and mitochondrial morphology and function, Ace Therapeutics provides services such as mitochondrial permeability transition pore assay and high-throughput sequencing.

Exploration of the Role of Mitochondria-Dependent Apoptosis in Stroke

In addition to being a source of cellular power, mitochondria are closely associated with many apoptosis-related proteins, such as the B-cell lymphoma (Bcl-2) family and apoptosis-inducing factors. For this function, Ace Therapeutics offers assays for pro-apoptotic factors such as Bax, Bak, cytochrome c, and nuclear endonuclease G, and anti-apoptotic factors such as Bcl-2, Bcl-xL, and Bcl-w.

If you would like to learn more about our services, please feel free to contact us.

1. Guan, R., et al., Mitophagy, a potential therapeutic target for stroke. J Biomed Sci, 2018. 25(1): p. 87.
2. Nguyen, H., et al., Understanding the role of dysfunctional and healthy mitochondria in stroke pathology and its treatment. Int J Mol Sci, 2018. 19(7).