Tuğba Aydıntuğ-Gürbüz, Fatih Toprak, Selin Toprak, Selçuk Sözer
{"title":"缺氧条件下 IGF1 和 MGF 对神经干细胞的影响","authors":"Tuğba Aydıntuğ-Gürbüz, Fatih Toprak, Selin Toprak, Selçuk Sözer","doi":"10.32598/bcn.2022.3981.1","DOIUrl":null,"url":null,"abstract":"<p><strong>Introduction: </strong>Ischemic stroke has high morbidity and mortality rates worldwide. Low oxygen (O<sub>2</sub>) 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. This study investigates the molecular and functional effects of growth factors, namely, insulin-like growth factor 1 (IGF-I) and mechano growth factor (MGF), in NSC exposed to low O<sub>2</sub> levels.</p><p><strong>Methods: </strong>An in vitro ischemia model was created by rat hippocampal NSC grown in culture that was exposed to varying oxygen levels, including 0%, 3%, and 20 % for the representation of anoxic, hypoxic, and normoxic conditions, respectively, during 24 h. NSC has investigated <i>IGF-I</i>, <i>MGF</i>, and <i>HIF1-Alpha (HIF-1α)</i> gene expressions by real-time reverse transcription polymerase chain reaction. The effects of external administration of growth factors (IGF-I and MGF) on NSC proliferation in such conditions were explored.</p><p><strong>Results: </strong>Increased <i>IGF-I</i> and <i>MGF</i> gene expressions were detected in the samples exposed to low O<sub>2</sub>. Anoxia was the highest stimulant for <i>IGF-I</i> and <i>MGF</i> gene expressions. Meanwhile, HIF1-α that encodes hypoxia-inducible factor-1α revealed downregulation in relative gene expression fold change with IGF-I application in all conditions, whereas <i>MGF</i> application upregulated its change in an anoxic environment. Furthermore, MGF-induced NSC had more proliferationmigration rate in all oxygen conditions. <i>IGF-I</i> induced significant NSC proliferation in 0% and 20% O<sub>2</sub>.</p><p><strong>Conclusion: </strong>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.</p>","PeriodicalId":8701,"journal":{"name":"Basic and Clinical Neuroscience","volume":null,"pages":null},"PeriodicalIF":1.0000,"publicationDate":"2024-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11470890/pdf/","citationCount":"0","resultStr":"{\"title\":\"The Effects of IGF1 and MGF on Neural Stem Cells in Hypoxic Conditions.\",\"authors\":\"Tuğba Aydıntuğ-Gürbüz, Fatih Toprak, Selin Toprak, Selçuk Sözer\",\"doi\":\"10.32598/bcn.2022.3981.1\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><strong>Introduction: </strong>Ischemic stroke has high morbidity and mortality rates worldwide. Low oxygen (O<sub>2</sub>) 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. This study investigates the molecular and functional effects of growth factors, namely, insulin-like growth factor 1 (IGF-I) and mechano growth factor (MGF), in NSC exposed to low O<sub>2</sub> levels.</p><p><strong>Methods: </strong>An in vitro ischemia model was created by rat hippocampal NSC grown in culture that was exposed to varying oxygen levels, including 0%, 3%, and 20 % for the representation of anoxic, hypoxic, and normoxic conditions, respectively, during 24 h. NSC has investigated <i>IGF-I</i>, <i>MGF</i>, and <i>HIF1-Alpha (HIF-1α)</i> gene expressions by real-time reverse transcription polymerase chain reaction. The effects of external administration of growth factors (IGF-I and MGF) on NSC proliferation in such conditions were explored.</p><p><strong>Results: </strong>Increased <i>IGF-I</i> and <i>MGF</i> gene expressions were detected in the samples exposed to low O<sub>2</sub>. Anoxia was the highest stimulant for <i>IGF-I</i> and <i>MGF</i> gene expressions. Meanwhile, HIF1-α that encodes hypoxia-inducible factor-1α revealed downregulation in relative gene expression fold change with IGF-I application in all conditions, whereas <i>MGF</i> application upregulated its change in an anoxic environment. Furthermore, MGF-induced NSC had more proliferationmigration rate in all oxygen conditions. <i>IGF-I</i> induced significant NSC proliferation in 0% and 20% O<sub>2</sub>.</p><p><strong>Conclusion: </strong>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. 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The Effects of IGF1 and MGF on Neural Stem Cells in Hypoxic Conditions.
Introduction: 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. This study investigates the molecular and functional effects of growth factors, namely, insulin-like growth factor 1 (IGF-I) and mechano growth factor (MGF), in NSC exposed to low O2 levels.
Methods: An in vitro ischemia model was created by rat hippocampal NSC grown in culture that was exposed to varying oxygen levels, including 0%, 3%, and 20 % for the representation of anoxic, hypoxic, and normoxic conditions, respectively, during 24 h. NSC has investigated IGF-I, MGF, and HIF1-Alpha (HIF-1α) gene expressions by real-time reverse transcription polymerase chain reaction. The effects of external administration of growth factors (IGF-I and MGF) on NSC proliferation in such conditions were explored.
Results: 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 gene expressions. Meanwhile, 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 proliferationmigration rate in all oxygen conditions. IGF-I induced significant NSC proliferation in 0% and 20% O2.
Conclusion: 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.
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BCN is an international multidisciplinary journal that publishes editorials, original full-length research articles, short communications, reviews, methodological papers, commentaries, perspectives and “news and reports” in the broad fields of developmental, molecular, cellular, system, computational, behavioral, cognitive, and clinical neuroscience. No area in the neural related sciences is excluded from consideration, although priority is given to studies that provide applied insights into the functioning of the nervous system. BCN aims to advance our understanding of organization and function of the nervous system in health and disease, thereby improving the diagnosis and treatment of neural-related disorders. Manuscripts submitted to BCN should describe novel results generated by experiments that were guided by clearly defined aims or hypotheses. BCN aims to provide serious ties in interdisciplinary communication, accessibility to a broad readership inside Iran and the region and also in all other international academic sites, effective peer review process, and independence from all possible non-scientific interests. BCN also tries to empower national, regional and international collaborative networks in the field of neuroscience in Iran, Middle East, Central Asia and North Africa and to be the voice of the Iranian and regional neuroscience community in the world of neuroscientists. In this way, the journal encourages submission of editorials, review papers, commentaries, methodological notes and perspectives that address this scope.
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