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. 2022 Jun;49(6):4435-4441.
doi: 10.1007/s11033-022-07283-7. Epub 2022 Mar 28.

Study of the influence of NGF-β gene overexpression in human mesenchymal stem cells on the expression level of SOX1 and neural pathway genes

Julia Morys  1 , Paulina Borkowska  2 , Aleksandra Zielinska  2 , Jan Kowalski  2
Affiliations

Study of the influence of NGF-β gene overexpression in human mesenchymal stem cells on the expression level of SOX1 and neural pathway genes

Julia Morys et al. Mol Biol Rep. 2022 Jun.

Abstract

Background: Nerve growth factor (NGF) is a protein exhibiting an influence on the neural development and also, its' impact on the stem cells remains a great potential treatment strategy. The influence of its overexpression on the neural pathway differentiation on Wharton's Jelly derived MSC (WJ-MSC) has not been studied so far, but considering the fact that these cells are relatively easy to obtain, using them may indicate an innovative change in stem cell therapies. The aim of this study was to evaluate the effect of NGF overexpression in human mesenchymal stem cells (MSC) on SOX1 and genes related to the neural pathway.

Methods and results: The lentiviral transduction was performed in order to obtain the NGF overexpression, as well as RT-PCR to evaluate the expression level SOX1, SOX2, NES, NGF under influence of overexpressed NGF protein in WJ-MSC. During the study we have observed a decrease in SOX1 expression as the marker of neural stem cells. Other than that an increase of SOX2, NES and NGF was noticed, as they all are markers of early-neural as well as already differentiated neural cells. The results show a great potential of using those examined genes' expression as a form of a new stem cell therapy.

Conclusions: The achieved overexpression of NGF in this study, led the modified MSC onto the neural pathway as well as caused a decrease of SOX1 expression and an increase of expression of genes related to neural differentiated cells.

Keywords: Differentiation; Lentiviral transduction; MSC; NGF; Neural pathway; Overexpression.

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