CN-121971618-A - Application of CDKN1A interaction zinc finger protein 1 in neuron axon regulation

Abstract

The invention discloses an application of CDKN1A interaction zinc finger protein 1 in neuron axon regulation. The invention provides and verifies that CDKN1A interaction zinc finger protein 1 can effectively regulate and control the growth behavior of neuron axons, inhibit the expression of the protein and promote the growth of the neuron axons and the regeneration of damaged axons, and provide a new direction for the research and development of medicaments for treating diseases caused by neurodegenerative diseases and nerve damage.

Inventors

• YI CHENG
• XIE JIALE
• YANG PENG
• SHEN YINYING

Assignees

• 南通大学

Dates

Publication Date

20260505

Application Date

20260209

Claims (10)

1. 1. Use of CDKN1A interacting zinc finger protein 1 in neuronal axon regulation.
2. 2. The use according to claim 1, wherein the use is to inhibit CDKN1A interacting zinc finger protein 1 expression to promote neuronal axon growth.
3. 3. The use according to claim 1, wherein the use is to inhibit CDKN1A interacting zinc finger protein 1 expression to promote neuronal damaged axon regeneration.
4. 4. The use according to claim 1, wherein the use is the use of a CDKN1A interacting zinc finger protein 1 expression inhibitor in the preparation of a medicament for the treatment of neurodegenerative diseases.
5. 5. The use according to claim 4, wherein said neurodegenerative diseases comprise alzheimer's disease, parkinson's disease, amyotrophic lateral sclerosis.
6. 6. The use according to claim 1, wherein the use is the use of a CDKN1A interacting zinc finger protein 1 expression inhibitor in the preparation of a medicament for the treatment of a disease caused by nerve damage.
7. 7. The use according to claim 4, wherein the disease caused by nerve damage comprises a disease caused by physical and/or physiological damage to nerves.
8. 8. The use according to any one of claims 4 to 7, wherein the inhibitor of CDKN1A interacting zinc finger protein 1 expression is any one of: a) siRNA, shRNA, sgRNA, miRNA, any one of which; b) A viral vector or a non-viral vector comprising a) or expressing a) in vivo; c) CDKN1A interacting zinc finger protein 1 nucleic acid aptamer or protein inhibitor.
9. 9. The use according to claim 8, wherein the inhibitor of CDKN1A interacting zinc finger protein 1 expression is a viral vector expressing shRNA.
10. 10. The use according to claim 9, wherein the viral vector is an adeno-associated viral vector or a lentiviral vector.

Description

Application of CDKN1A interaction zinc finger protein 1 in neuron axon regulation Technical Field The invention relates to gene therapy, in particular to application of CDKN1A interaction zinc finger protein 1 in neuron axon regulation. Background Neuronal axons are elongated processes used by neurons for signaling, whose growth and regeneration are central to the development of the nervous system, repair of injury, and functional remodeling. During the developmental stage, the cytoskeleton of the axon tip growth cone directs its precise extension. However, the ability to regenerate after axonal injury in the central nervous system is extremely weak in adult mammals. Therefore, it is a key to promote nerve repair after spinal cord injury and other diseases to explore how to reactivate the intrinsic growth potential of neurons and improve the external environment. Dorsal root ganglion neurons are classical models for studying the mechanism of axon regeneration. As a pseudo-monopolar neuron, the unique anatomical structure provides a natural control for researching the regeneration capability difference, namely the regeneration capability of the peripheral process is strong after injury, and the peripheral process hardly regenerates after injury of the central process projected to the spinal cord. Furthermore, the ability of DRG neurons to regenerate decreases with age, but studies have found that administration of specific growth factors is effective in stimulating their axonal regeneration potential even in older animals, which holds promise for treatment. CDKN1A interacting zinc finger protein 1 (CIZ 1) is a protein that functions primarily in the nucleus and plays a key role in DNA replication and in the regulation of checkpoints during the G1/S phase of the cell cycle. Studies have shown that CIZ1 is critical for maintaining genomic stability and that its functional defects can lead to DNA damage accumulation, cell cycle abnormalities and apoptosis. The current research also focuses mainly on the DNA-related function of CIZ1 in the nucleus, and it is currently unclear whether it may affect the growth and regeneration of neuronal axons. Disclosure of Invention The invention aims to provide an application of CDKN1A interaction zinc finger protein 1 in neuron axon regulation, in particular to an application of inhibiting CDKN1A interaction zinc finger protein 1 to promote neuron axon growth or injury repair. The technical scheme is that the CDKN1A interaction zinc finger protein 1 is applied to neuron axon regulation. Preferably, the use is to inhibit CDKN1A interacting zinc finger protein 1 expression to promote neuronal axon growth. Preferably, the use is to inhibit CDKN1A interacting zinc finger protein 1 expression to promote regeneration of a neuronal damaged axon. Preferably, the application is the application of the CDKN1A interaction zinc finger protein 1 expression inhibitor in preparing medicaments for treating neurodegenerative diseases, and more preferably, the neurodegenerative diseases comprise Alzheimer disease, parkinson disease and amyotrophic lateral sclerosis. Preferably, the application is the application of the CDKN1A interaction zinc finger protein 1 expression inhibitor in preparing a medicament for treating diseases caused by nerve injury, and more preferably, the diseases caused by nerve injury comprise diseases caused by physical and/or physiological injury of nerves. Preferably, the inhibitor of CDKN1A interacting zinc finger protein 1 expression is any one of: a) siRNA, shRNA, sgRNA, miRNA, any one of which; b) A viral vector or a non-viral vector comprising a) or expressing a) in vivo; c) CDKN1A interacting zinc finger protein 1 nucleic acid aptamer or protein inhibitor. Preferably, the CDKN1A interacting zinc finger protein 1 expression inhibitor is a viral vector for expressing shRNA, and more preferably, the viral vector is an adeno-associated viral vector or a lentiviral vector. Compared with the prior art, the invention has the following remarkable advantages that the CDKN1A interaction zinc finger protein 1 can effectively regulate and control the neurite of the neuron, inhibit the expression of the neurite and promote the growth of the neurite and the regeneration of the damaged neurite, and provide a new direction for the research and development of medicaments for treating diseases caused by neurodegenerative diseases and nerve injury. Drawings FIG. 1 is a diagram showing Ciz1 expression after injury to sciatic nerve (A) or dorsal root (B) in rats; FIG. 2 is a graph showing Ciz1 expression after infection of rat DRG neurons with different adeno-associated viruses; FIG. 3 is a graph of neurite outgrowth following infection of rat DRG neurons with different adeno-associated viruses; FIG. 4 is a graph showing regeneration of the neurites after disruption of the neurites after infection of rat DRG neurons with different adeno-associated viruses; FIG. 5 is a graph showing im