Accepted Articles                   Back to the articles list | Back to browse issues page

XML Print

1- Department of Genetics, Aziz Sancar Research Institute of Experimental Medicine, Istanbul University
2- Department of Neurosurgery, Haydarpaşa Numune Training and Research Hospital

Ischemic stroke has high morbidity and mortality rates worldwide. Low oxygen (O2) levels detected in such conditions create a vulnerable environment for neural stem cells (NSC), altering neuronal function and leading to neuronal injury or death. There are still no effective treatments for such consequences. We have investigated the molecular and functional effects of growth factors, IGF-I and MGF in NSC exposed to low O2 levels. An in vitro ischemia model was created by rat hippocampal NSC grown in culture that were exposed to varying oxygen levels including 0%, 3%, and 20 % for the representation of anoxic, hypoxic, and normoxic conditions, respectively, during the 24 hours. NSC was investigated for IGF-I, MGF, and HIF1-Alpha (HIF-1α) gene expressions by real-time RT-PCR. The effects of external administration of growth factors, IGF-I and MGF on NSC proliferation in such conditions were explored. Increased IGF-I and MGF gene expressions were detected in the samples exposed to low O2. Anoxia was the highest stimulant for IGF-I and MGF expressions. HIF1-α that encodes hypoxia-inducible factor-1α revealed downregulation in relative gene expression fold change with IGF-I application in all conditions, whereas MGF application upregulated its change in an anoxic environment. Furthermore, MGF-induced NSC had more proliferation- migration rate in all oxygen conditions. IGF-I induced significant NSC proliferation in 0% and 20% O2. These findings suggest that IGF-I and MGF expressions were increased to reduce the damage in NSC exposed to low oxygen, and exogenous MGF and IGF-I application increased NSC proliferation at the time of injury. The results might imply the role of exogenous MGF and IGF-I in the treatment of ischemia for relieving the effect of neuronal damage due to their neuroprotective and proliferative effects.

Type of Study: Original | Subject: Cellular and molecular Neuroscience
Received: 2022/02/8 | Accepted: 2022/09/21

Add your comments about this article : Your username or Email:

Send email to the article author

Rights and permissions
Creative Commons License This work is licensed under a Creative Commons Attribution-NonCommercial 4.0 International License.

© 2024 CC BY-NC 4.0 | Basic and Clinical Neuroscience

Designed & Developed by : Yektaweb