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| Status |
Public on Aug 01, 2024 |
| Title |
Perinatal Brain Injury Triggers Niche-Specific Changes to Cellular Biogeography [MERFISH] |
| Platform organism |
synthetic construct |
| Sample organism |
Mus musculus |
| Experiment type |
Other
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| Summary |
Preterm infants are at risk for brain injury and long term neurodevelopmental impairment due, in part, to white matter injury following chronic hypoxia exposure. However, the precise molecular mechanisms by which perinatal hypoxia disrupts early neurodevelopment are poorly understood. Here, we constructed a brain-wide map of the regenerative response to newborn brain injury using high resolution imaging-based spatial transcriptomics (MERFISH) to analyze over 1.3 million cells in a mouse model of chronic neonatal hypoxia. We also developed a new method for inferring condition-associated differences in cell type spatial proximity, enabling the identification of niche-specific changes in cellular architecture. We observed significant hypoxia-associated changes in region-specific cell states, cell type composition, and spatial organization. Our findings suggest that perinatal hypoxia disrupts oligodendrocyte formation and crosstalk signaling with other cell types in their niche. Importantly, our analysis of spatially-informed gene expression patterns revealed specific mechanisms of reparative neurogenesis and gliogenesis, and nominated pathways that may impede circuit rewiring following perinatal hypoxia. Altogether, our work provides a comprehensive description of the brain-wide response to newborn brain injury and identifies candidate signaling pathways for functional interrogation.
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| Overall design |
Multiplexed error-robust fluorescence in situ hybridization (MERFISH) was performed on postnatal day 21 (P21) mice from two conditions: 1) mice that were exposed to 21% oxygen during development (normoxia), 2) mice that were exposed to 10% oxygen (hypoxia) between P3-P11. Coronal sections of the entire brain were used for analysis.
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| Contributor(s) |
Tahmasian N, Feng MY, Arbabi K, Rusu B, Cao W, Kukreja B, Tripathy S, Kalish BT |
| Citation missing |
Has this study been published? Please login to update or notify GEO. |
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| Submission date |
Feb 15, 2024 |
| Last update date |
Aug 01, 2024 |
| Contact name |
Brian Kalish |
| E-mail(s) |
brian.kalish@sickkids.ca
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| Phone |
6305329007
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| Organization name |
Harvard Medical School
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| Department |
Neurobiology
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| Lab |
Greenberg Lab
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| Street address |
220 Longwood Ave
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| City |
Boston |
| State/province |
MA |
| ZIP/Postal code |
02115 |
| Country |
USA |
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| Platforms (1) |
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| Samples (6)
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| GSM8082299 |
Postnatal day 21 (P21) hypoxia, biological rep 1 |
| GSM8082300 |
Postnatal day 21 (P21) hypoxia, biological rep 2 |
| GSM8082301 |
Postnatal day 21 (P21) hypoxia, biological rep 3 |
| GSM8082302 |
Postnatal day 21 (P21) normoxia, biological rep 1 |
| GSM8082303 |
Postnatal day 21 (P21) normoxia, biological rep 2 |
| GSM8082304 |
Postnatal day 21 (P21) normoxia, biological rep 3 |
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| Relations |
| BioProject |
PRJNA1076924 |
| Supplementary file |
Size |
Download |
File type/resource |
| GSE255892_RAW.tar |
13.2 Gb |
(http)(custom) |
TAR (of CSV) |
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