التفاصيل البيبلوغرافية
العنوان: |
Mecp2 knock-out astrocytes affect synaptogenesis by interleukin 6 dependent mechanisms |
المؤلفون: |
Elena Albizzati, Martina Breccia, Elena Florio, Cecilia Cabasino, Francesca Maddalena Postogna, Riccardo Grassi, Enrica Boda, Cristina Battaglia, Clara De Palma, Concetta De Quattro, Davide Pozzi, Nicoletta Landsberger, Angelisa Frasca |
المصدر: |
iScience, Vol 27, Iss 3, Pp 109296- (2024) |
بيانات النشر: |
Elsevier, 2024. |
سنة النشر: |
2024 |
المجموعة: |
LCC:Science |
مصطلحات موضوعية: |
Cell biology, Immunology, Neuroscience, Omics, Transcriptomics, Science |
الوصف: |
Summary: Synaptic abnormalities are a hallmark of several neurological diseases, and clarification of the underlying mechanisms represents a crucial step toward the development of therapeutic strategies. Rett syndrome (RTT) is a rare neurodevelopmental disorder, mainly affecting females, caused by mutations in the X-linked methyl-CpG-binding protein 2 (MECP2) gene, leading to a deep derangement of synaptic connectivity. Although initial studies supported the exclusive involvement of neurons, recent data have highlighted the pivotal contribution of astrocytes in RTT pathogenesis through non-cell autonomous mechanisms. Since astrocytes regulate synapse formation and functionality by releasing multiple molecules, we investigated the influence of soluble factors secreted by Mecp2 knock-out (KO) astrocytes on synapses. We found that Mecp2 deficiency in astrocytes negatively affects their ability to support synaptogenesis by releasing synaptotoxic molecules. Notably, neuronal inputs from a dysfunctional astrocyte-neuron crosstalk lead KO astrocytes to aberrantly express IL-6, and blocking IL-6 activity prevents synaptic alterations. |
نوع الوثيقة: |
article |
وصف الملف: |
electronic resource |
اللغة: |
English |
تدمد: |
2589-0042 |
Relation: |
http://www.sciencedirect.com/science/article/pii/S2589004224005170; https://doaj.org/toc/2589-0042 |
DOI: |
10.1016/j.isci.2024.109296 |
URL الوصول: |
https://doaj.org/article/6450361ee82f407ab22cd269cc2ed3c1 |
رقم الانضمام: |
edsdoj.6450361ee82f407ab22cd269cc2ed3c1 |
قاعدة البيانات: |
Directory of Open Access Journals |