Final, sorry: Gene And Microglia Mediate Early Synapse Loss
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Gene And Microglia Mediate Early Synapse Loss - was and
Recognition of environmental cues is essential for the survival of all organisms. Transcriptional changes occur to enable the generation and function of the neural circuits underlying sensory perception. To gain insight into these changes, we generated single-cell transcriptomes of Drosophila olfactory- ORNs , thermo-, and hygro-sensory neurons at an early developmental and adult stage using single-cell and single-nucleus RNA sequencing. We discovered that ORNs maintain expression of the same olfactory receptors across development. Using receptor expression and computational approaches, we matched transcriptomic clusters corresponding to anatomically and physiologically defined neuron types across multiple developmental stages. We found that cell-type-specific transcriptomes partly reflected axon trajectory choices in development and sensory modality in adults. We uncovered stage-specific genes that could regulate the wiring and sensory responses of distinct ORN types. Collectively, our data reveal transcriptomic features of sensory neuron biology and provide a resource for future studies of their development and physiology.
Glioma-associated microglial cells, a key component of the tumor microenvironment, play an important role in glioma progression. In this study, the mouse glioma cell line GL and the mouse microglia cell line BV2 were chosen.
Introduction
First, circadian gene expression in glioma cells co-cultured with either M1 or M2 microglia was assessed and the exosomes of M2-polarized and unpolarized BV-2 microglia were extracted. Subsequently, we labeled the exosomes with PKH67 and treated GL cells with them to investigate the exosome distribution.
GL cell phenotypes and related protein expression were used to explore the role of M2 microglial exosomes in gliomas. Then a specific miRp inhibitor was added to verify miRp functions. Finally, the mouse subcutaneous tumorigenic model was used to verify the tumorigenic effect of M2 microglial exosomes in vivo. Increased expression of N-cadherin and Vimentin, and decreased E-cadherin expression occurred upon treatment with M2 microglial exosomes. Addition of an miRp inhibitor to M2 microglial exosomes reversed these results.
In Mrdiate, we found that miRp in the glioma microenvironment is recruited to glioma cells by exosomes and inhibits Bmal1 expression. M2 microglial exosomes promote the proliferation and migration of gliomas by regulating tumor-related protein expression and reducing apoptosis.
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Glioma is the most common primary tumor in the central nervous system CNS. The prognosis of glioma patients is closely related article source the degree of malignancy.
Currently, the prognosis of high-grade glioma patients is still not optimistic [ 1 ]. According to their biological functions, GAMs have been shown to polarize into two distinct phenotypes: M1 microglia that inhibit tumor progression and M2 microglia that function in the opposite way [ 345 ]. Exosome miRNAs, as important mediators of communication in multiple pathological environments, are involved in frequent two-way communication between tumor Synapwe and the TME [ 67 ].
Recently, based on the rapid development of biotechnology, especially the high-throughput sequencing, the mechanism of TME regulation has been increasingly investigated. Recent results indicate that, as an important participant in epigenetic regulation, miRNAs are involved in a variety Eaarly diseases, including cancers [ 8910 ].
Original Research ARTICLE
However, due to the complexity of the TME, the interaction between glioma and microglia in the TME, as well as the regulatory mechanism of exosomal miRNAs in specific physiological systems, still need further study. As one of the most basic physiological regulation systems, the circadian rhythm system, participates in various human biological and physiological activities and maintains internal homeostasis. Therefore, disorder of the circadian rhythm system tends to result in a dysregulated internal environment and causes diseases [ 111213 ]. Due to the complexity and universality of the circadian rhythm system, the study of its molecular mechanism is challenging. Although increasing evidence suggests that circadian dysregulation affects the immune system [ 1415 ], the exact mechanism of the interaction between miRNAs, clock genes, and glioma progression remains unclear.
INTRODUCTION
In this study, we explored the hypothesis that microglia regulate the expression of glioma clock genes source exosomes, leading to promotion of the proliferation and metastasis of glioma. As a core gene of the circadian rhythm system, Bmal1 has been associated with the development of multiple types of tumors. Therefore, Ans miRNAs that can regulate Bmal1 is of great importance for elucidating the molecular mechanism by which M2 microglia promote glioma progression, and to provide a theoretical basis for the development of biologically-targeted therapy for glioma.]
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