Cross-Talk Between Exogenous Growth Factors and Endogenous Growth Factors Released from Astroglial-Conditioned Media onDNA and RNA Labeling and ERK1/2 Expression in Astrocytesin an in Vitro Model
DOI:
https://doi.org/10.47363/JPSRR/2025(7)198Keywords:
Expression, Growth FactorsAbstract
The aim of this present investigation is to study the cross-talk between exogenous growth factors and endogenous growth factors released from astroglialconditioned media on DNA and RNA labeling and ERK ½ expression in astrocytes in an in vitro model. To better clarify mechanism of astroglial cell proliferation /differentiation in culture, incorporation of [methyl-3H]-thymidine or [5,6-3H]-uridine in astroglial cell cultures was investigated. Astrocytes cultures were pre-treated with Epidermal Growth Factor (EGF), insulin (INS), Insulin-Like Growth Factor-I (IGF- I), and Basic Fibroblast Growth Factor (bFGF) and subsequently with Astroglial Conditioned Media (ACM). In particular, the incorporation of [methyl-3H]-thymidine into DNA showed a significant increase in ACM from 15 days in vitro (DIV) cultures in 30 DIV astrocytes after12 h pre-treatment with growth factors. The pre-treatment with INS or EGF in 30 DIV astrocytes cultures was showed.
ACM collected from 15 or 60 or 90 DIV increased the [5,6-3H] uridine incorporation into RNA of 15 and 30 DIV astrocyte cultures. Increase in RNA labeling of 30 DIV cultures added with ACM from 90 DIV was obtained. The results of enhancement in DNA labeling after pre- treatment with EGF or INS in 30 DIV astrocytes cultures and subsequent addition of ACM from 15 DIV cultures, indicate that the involvement may depend on Extra Cellular SignalRegulated Kinase (ERK1) activation. In summary, the environment created by astroglial cultures can regulate their own proliferation and differentiation, through the release of soluble mediators finally acting on their genomic program. This may be relevant in vivo, when scheduled events related to brain development are regulated by astrocyte-derived growth factors controlling neuronal and glial architecture from the postnatal period until the adulthood.
