The Role of MARK ERK1/2 and p38 in Regulation of Functions of Neural Stem Cells and Neuroglia under Conditions of β-Amyloid-Induced Neurodegeneration

Abstract

The role of ERK1/2 and p38 in the realization of the growth potential of neural stem cells and secretion of neurotrophic growth factors by glial cells was studied using in vitro model of β-amyloid-induced neurodegeneration. It was shown that amyloid-β fragment 25-35 significantly inhibits the cell cycle progression of neural stem cells against the background of stimulation of their differentiation and reduced production of growth factors by neuroglia. The inhibitory role of ERK1/2 and p38 in relation to the proliferative activity of neural stem cells and the secretory activity of glial elements was revealed. ERK1/2 and p38 inhibitors increased proliferation of progenitor cells of the nervous tissue and reduced the intensity of their specialization, as well as stimulated production of growth factors by neuroglial cells under conditions of simulated β-amyloid-induced neurodegeneration.

Quercetin-3-O-β-d-glucuronide in the Nuciferine Leaf Polyphenol Extract Promotes Neurogenesis Involving the Upregulation of the Tropomyosin Receptor Kinase (Trk) Receptor and AKT/Phosphoinositide 3-Kinase Signaling Pathway

“…In the aging process, NGF deprivation or NGFR loss also leads to cell cycle deficit . A study indicated that β-amyloid inhibits the cell cycle progression of NSC and reduces the production of growth factor . Therefore, in addition to reducing neuronal cell death, increasing cell viability is an alternative treatment option for neurodegeneration.…”

“…34 A study indicated that β-amyloid inhibits the cell cycle progression of NSC and reduces the production of growth factor. 35 Therefore, in addition to reducing neuronal cell death, increasing cell viability is an alternative treatment option for neurodegeneration. Sang proposed that the NGF and the PI3K/Akt signaling pathway participate in neuroprotection and curcumin upregulates this pathway.…”