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LAG3 regulates the homeostasis of brain white matter microglia and affects astrocyte morphogenesis in the early postnatal period

ABSTRACT: LAG3 regulates the homeostasis of brain white matter microglia and affects astrocyte morphogenesis in the early postnatal period

PROVIDER: PRJNA1165146 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR30791868.fastq.gz	Fastqsanger.gz
	SRR30791869.fastq.gz	Fastqsanger.gz
	SRR30791870.fastq.gz	Fastqsanger.gz
	SRR30791871.fastq.gz	Fastqsanger.gz

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LAG3 regulates the homeostasis of brain white matter microglia and affects astrocyte morphogenesis in the early postnatal period

Project description:In order to further understand how microglia-derived LAG3 regulates microglia homeostasis and affects the morphogenesis of astrocytes, RNA-seq was used to analyze the transcriptome changes of microglia isolated from Lag3 conditional knockout mice and littermate-born wild-type mice in P7 period. About 7000 transcripts showed the differential expression between the microglia of the corpus callosum of Lag3fl/fl and Lag3cKO-Cx3 mice, with a fold change ≥2, and a p value < 0.05. Geneontology analysis of downregulated genes were enriched in terms related to actin recombination, ciliary recombination and others, while upregulated genes are enriched in inflammatory response and other terms. These results reflected the role of microglia Lag3 in microglia development.

2024-09-30 | GSE277980 | GEO

Astrocyte morphogenesis is dependent on BDNF signaling via astrocytic TrkB.T1

Project description:Astrocytic morphogenesis and maturation are critical steps in CNS development. The time window of astrocyte morphological development is well defined, but the molecular underpinnings are still unclear. BDNF is a critical growth factor involved in the development of the CNS, including synapse refinement. Here we demonstrate the BDNF receptor at Ntrk2 is enriched in astrocytes relative to all CNS cell populations. RNA sequencing indicates Ntrk2 falls in the top 0.001% of all gene transcripts expressed in juvenile astrocytes, almost exclusively due to truncated TrkB.T1. Astrocyte complexity is increased in the presence of BNDF in vitro, which is dependent upon the presence of TrkB.T1. Furthermore, deletion of TrkB.T1 in vivo revealed astrocytes with significantly reduced volume and branching complexities. Indicating a role for functional astrocyte maturation via BDNF/TrkB.T1 signaling, TrkB.T1 KO astrocytes do not support normal excitatory synaptogenesis. Together, these data suggest a significant role for BDNF/TrkB.T1 signaling in astrocyte morphogenesis and indicate this signaling may contribute to astrocyte regulation of neuronal synapse development.

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Inhibitory input directs astrocyte morphogenesis through glial GABABR

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Astroglial Hmgb1 regulates postnatal astrocyte morphogenesis and cerebrovascular maturation

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Astroglial Hmgb1 regulates postnatal astrocyte morphogenesis and cerebrovascular maturation

Project description:Astroglial Hmgb1 regulates postnatal astrocyte morphogenesis and cerebrovascular maturation

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Astrocyte morphogenesis is dependent on BDNF signaling via astrocytic TrkB.T1

Project description:Astrocyte morphogenesis is dependent on BDNF signaling via astrocytic TrkB.T1

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Inhibitory input directs astrocyte morphogenesis through glial GABABR [scRNA-Seq]

Project description:Inhibitory input directs astrocyte morphogenesis through glial GABABR [scRNA-Seq]

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Transcription profiling of mouse CD4+ CD25+, CD4+ CD25- CD45RBlow LAG3+ and CD4+ CD25- CD45RBlow LAG3- T cells

Project description:Comparison of gene expression profile of CD4+ CD25+, CD4+ CD25- CD45RBlow LAG3+ and CD4+ CD25- CD45RBlow LAG3- T cells. Naive CD4+CD25-CD45RBhigh T cells were used as a reference for pair comparison with values from the three other subsets.

2009-08-19 | E-MEXP-1343 | biostudies-arrayexpress

Inhibitory input directs astrocyte morphogenesis through glial GABABR [bulk RNA-Seq]

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Lymphocyte activation gene 3 (Lag3) supports Foxp3+ Treg cell function by restraining c-Myc-dependent aerobic glycolysis

Project description:Lymphocyte activation gene 3 (Lag3) has emerged as the next-generation immune checkpoint molecule due to its ability to inhibit effector T cell activity. Foxp3+ regulatory T (Treg) cells, a master regulator of immunity and tolerance, also highly express Lag3. While Lag3 is thought to be necessary for Treg cell-mediated regulation of immunity, the precise roles and underlying mechanisms remain largely elusive. In this study, we report that Lag3 is indispensable for Treg cells to control autoimmune inflammation. Utilizing a newly generated Treg cell specific Lag3 mutant mouse model, we found that these animals are highly susceptible to autoimmune diseases, suggesting defective Treg cell function. Genome wide transcriptome analysis further uncovered that Lag3 mutant Treg cells upregulated genes involved in metabolic processes. Mechanistically, we found that Lag3 limits Treg cell expression of Myc, a key regulator of aerobic glycolysis. We further found that Lag3-dependent Myc expression determines Treg cells’ metabolic programming as well as the in vivo function to suppress autoimmune inflammation. Taken together, our results uncovered a novel function of Lag3 in supporting Treg cell suppressive function by regulating Myc-dependent metabolic programming.

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