Rattus norvegicus
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ABSTRACT:
PROVIDER: PRJNA140741 | ENA |
REPOSITORIES: ENA
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Project description:Microglia, the resident immune cells of the central nervous system (CNS), have two distinct phenotypes in the developing brain: amoeboid form, known to be amoeboid microglial cells (AMC) and ramified form, known to be ramified microglial cells (RMC) alongside several intermediate forms. The AMC are characterized by being proliferative, phagocytic and migratory whereas the RMC are quiescent and exhibit a slow turnover rate. The AMC transform into RMC with advancing age, and this transformation is indicative of the gradual shift in the microglial functions. Both AMC and RMC respond to CNS inflammation, and they become hypertrophic when they are activated by trauma, infection or neurodegenerative stimuli. The molecular mechanisms and functional significance of morphological transformation of microglia during normal development and in disease conditions is not clear. It is hypothesized that AMC and RMC are functionally regulated by a specific set of genes encoding various signaling molecules and transcription factors. To address this, we carried out cDNA microarray analysis using lectin-labeled AMC and RMC isolated from frozen tissue sections of the corpus callosum of 5-day and 4-week old rat brain respectively, by laser capture microdissection (LCM). The global gene expression profiles of both microglial phenotypes were compared and the differentially expressed genes in AMC and RMC were clustered based on their functional annotations. This genome wide comparative analysis helps in identifying genes that are specific to AMC and RMC. The novel and specific molecules identified in both microglial phenotypes can be targeted for therapeutic purposes in developing and adult brain diseases. We used microarrays to identify the genes specific to amoeboid and ramified microglia. RNA was isolated from the laser-captured amoeboid and ramified microglia from the corpus callosum of 5-day and 4-week old rat brain. The RNA was hybridised onto Affymetrix Rat 230 2.0 array.
2011-06-11 | E-GEOD-29885 | biostudies-arrayexpress
Project description:Recently we demonstrated that amoeboid microglia in white matter regions are essential for proper oligodendrocyte homeostasis and myelinogenesis in the first postnatal week of mice. Amoeboid microglia in the corpus callosum change their activation profile already within few days after postnatal day (P)7 and microglia of the cerebellum show similar features to callosal microglia. Here we expanded our previous transcriptional analysis and performed bulk RNA sequencing of microglia during development in a detailed way in P7, P10 and P42 microglia from corpus callosum, cortex and cerebellum. The goal of this study was to identify a specific gene profile for both, white matter and grey matter microglia during development.
2020-04-10 | GSE132688 | GEO
Project description:Microglia, the resident immune cells of the central nervous system (CNS), have two distinct phenotypes in the developing brain: amoeboid form, known to be amoeboid microglial cells (AMC) and ramified form, known to be ramified microglial cells (RMC) alongside several intermediate forms. The AMC are characterized by being proliferative, phagocytic and migratory whereas the RMC are quiescent and exhibit a slow turnover rate. The AMC transform into RMC with advancing age, and this transformation is indicative of the gradual shift in the microglial functions. Both AMC and RMC respond to CNS inflammation, and they become hypertrophic when they are activated by trauma, infection or neurodegenerative stimuli. The molecular mechanisms and functional significance of morphological transformation of microglia during normal development and in disease conditions is not clear. It is hypothesized that AMC and RMC are functionally regulated by a specific set of genes encoding various signaling molecules and transcription factors. To address this, we carried out cDNA microarray analysis using lectin-labeled AMC and RMC isolated from frozen tissue sections of the corpus callosum of 5-day and 4-week old rat brain respectively, by laser capture microdissection (LCM). The global gene expression profiles of both microglial phenotypes were compared and the differentially expressed genes in AMC and RMC were clustered based on their functional annotations. This genome wide comparative analysis helps in identifying genes that are specific to AMC and RMC. The novel and specific molecules identified in both microglial phenotypes can be targeted for therapeutic purposes in developing and adult brain diseases. We used microarrays to identify the genes specific to amoeboid and ramified microglia.
2011-06-11 | GSE29885 | GEO
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Project description:Expression data from 9-day-old rat Sertoli cells and MBP-treated rat Sertoli cells
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Project description:Mkx ChIP-seq data of tendon-derived cells from 3-week-old Mkx-/- rat
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Project description:Whereas microglia involvement in virtually all brain diseases is well accepted their role for the control of homeostasis in the central nervous system (CNS) is mainly thought to maintain neuronal function through the formation, refinement and monitoring of synapses in both the developing and adult brain. Although the prenatal origin and the neuron-centered function of cortical microglia has recently been elucidated much less is known about a distinct amoeboid microglia population formerly described as “fountain of microglia” that appear only postnatally in the myelinating regions such as corpus callosum and cerebellum. Using large-scale transcriptional profiling, fate-mapping and genetic targeting approaches we identified a unique molecular signature of this microglia subset that arose from a CNS endogenous microglia pool independent from circulating myeloid cells. Microglia depletion experiments unexpectedly revealed an essential role of postnatal microglia for the proper development and homeostasis of oligodendrocytes. Our data provide new cellular and molecular insights into the myelin-supporting function of microglia in the normal CNS.
2017-07-19 | GSE96623 | GEO