The Role of JNK and p53 in the Regulation of Secretory Function of Neuroglial Cells of Various Types in β-Amyloid-Induced Neurodegeneration

• Published in: Bulletin of experimental biology and medicine Vol. 175; no. 6; pp. 753 - 756
• Main Authors: Zyuz’kov, G. N., Miroshnichenko, L. A., Chaikovskii, A. V., Kotlovskaya, L. Yu
• Format: Journal Article
• Language: English
• Published: New York Springer US 01.10.2023; Springer Nature B.V
• Subjects: Astrocytes; Biomedical and Life Sciences; Biomedicine; Cell Biology; Cell culture; Dementia; Glial cells; Growth factors; Internal Medicine; Kinases; Laboratory animals; Laboratory Medicine; Microglial cells; Neural stem cells; Neurodegeneration; Neurogenesis; Neurotoxicity; Neurotrophic factors; Oligodendrocytes; Pathology; Physiology; Proteins; Regenerative medicine; Signal transduction; Stem cells; Test systems; β-Amyloid; Alzheimer’s disease; neural stem cells; JNK; β-amyloid; p53
• ISSN: 0007-4888; 1573-8221
• DOI: 10.1007/s10517-023-05939-3

We studied the effect of JNK and p53 inhibitors on the production of neurotrophic factors stimulating the realization of the growth potential of neural stem cells by neuroglial cells of various types under conditions of simulation of induced β-amyloid neurodegeneration in vitro . It was shown that β-amyloid stimulates the production of neurotrophins by astrocytes and microglial cells, but does not affect the functioning of oligodendrocytes. JNK and p53 were not involved in the secretion of neurotrophins by intact astrocytes. The stimulating role of p53 on the implementation of their secretory activity under the influence of a neurotoxic agent was revealed. At the same time, the inhibitory role of JNK and p53 in the production of neurotrophic growth factors by oligodendrocytes and microglial cells was revealed both under conditions of their optimal vital activity and when β-amyloid was added to the cell culture.