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Inhibition of Sema-3A Promotes Cell Migration, Axonal Growth, and Retinal Ganglion Cell Survival
Anat Nitzan1, Miriam Corredor-Sanchez2, Ronit Galron1
1Department of Neurobiology, George S. Wise, Faculty of Life Sciences, Tel Aviv University, Tel Aviv, Israel.
Translational Vision Science & Technology
|November 24, 2021
Summary
Researchers developed novel Semaphorin 3A (Sema-3A) inhibitors, including antibodies and small molecules, for neuroprotection. These inhibitors, delivered via implants, successfully protected retinal ganglion cells in animal models, offering a promising therapeutic strategy for CNS degenerative diseases.
Area of Science:
- Neuroscience
- Immunology
- Pharmacology
Background:
- Semaphorin 3A (Sema-3A) is a protein that can cause neuronal cell death and axon misguidance.
- Inhibiting Sema-3A shows potential for neuroprotection, particularly for retinal ganglion cells after optic nerve injury.
Purpose of the Study:
- To develop potent and specific antagonists of Semaphorin 3A (Sema-3A).
- To evaluate the therapeutic potential of these Sema-3A inhibitors for neuroprotection.
Main Methods:
- Isolated monoclonal anti-Sema-3A antibodies from a human antibody phage display library.
- Optimized low-molecular weight Sema-3A signaling inhibitors.
- Formulated inhibitors in extruded implants for controlled, prolonged release.
- Assessed inhibitor efficacy using in vitro assays and animal models of optic nerve injury, retinal ischemia, and glaucoma.
Main Results:
- Developed effective Sema-3A inhibitors (antibodies and small molecules).
- Formulated inhibitors demonstrated prolonged release from implants.
- Inhibitors successfully antagonized Sema-3A effects in vitro.
- Retinal ganglion cells were protected in vivo in models of optic nerve injury, ischemia, and glaucoma.
Conclusions:
- Identified Sema-3A inhibitors warrant further investigation as therapeutic candidates.
- These inhibitors show promise for treating Sema-3A-driven central nervous system degenerative conditions.
- The development of sustained-release formulations enhances therapeutic potential.
